2018 KASBP Spring Symposium Program v3 Spring... · 2018. 6. 4. · SeanKim, Jae Uk Jeong Website and SNS Management Committee Daeho Lee Sahee Kim, Sohyun Aria Rhee, Jiyoung Jamie

P R O G R A M

KASBP SPONSORS

Korean-American scientists & engineers here in the United States.

Professional Association Meeting

US-Korea Joint Meeting

KAIST-KUSCO S&T Policy Workshop

Workshop for Korean R&D Managers

and Administrators

S&T Innovative Infrastructure

Development Program

NOAA-MOF JPA Program

Developing Infrastructur

for S&T Professionals

KUSCO Programs are composed of three categories;

Nurturing Human Resource & Exchage,

Strengthening S&T Cooperation,

and Developing Infrastructure for

S&T Professionals.

Preliminary Program

For more information, please visit www.kasbp.org

Welcoming Letter to 2018 KASBP Spring Symposium

Korean American Society in Biotech and Pharmaceuticals (KASBP) cordially invites all members and friends to the

2018 KASBP Spring Symposium, Co-hosted by Yuhan Corporation, Hanmi Pharmaceuticals, GC Pharma, Qurient and

KUSCO in Boston from June 1 to June 2, 2018, focused on Finding a Target in Drug Discovery and Development.

For the upcoming event, the symposium organizing committee is delighted to announce the recruitment of

outstanding speakers and panelists, including our distinguished keynote speaker, Dr. Peter J. Park, a world-renowned

Computational Genomics researcher and Professor of Biomedical Informatics from Harvard Medical School. This will

be a great opportunity to learn how computational and statistical analyses of genomics data are helping to identify

rare mutations in genome and to foster new discovery.

We are also fortunate to have seven distinguished speakers from both academia and industry who will share their

experience and expertise regarding cutting-edge science, process from the early discovery research to the clinical

trials and biopharmaceuticals. We will hear about the drug discovery challenges for Antibody-Drug Conjugate (ADC),

the evolution of medicinal chemistry that lead to the discovery of newly approved breast cancer therapy, KISQALI®,

and biologics platform for immuno-oncology. In addition, we will learn about nutrient sensing as new target for

aging, the application of modeling and simulation for preclinical and clinical studies, as well as how best prepare the

interaction with FDA for pre-IND and IND submission. Beyond these scientific topics, the first-hand experience in

building a biotechnology company will also be presented.

On Saturday evening, we will host a session titled Let’s License Out to hear several companies from Korea and US

about their product and services. Similar to last Fall’s Biotech Start Up Companies session, we will hold a

challenging session to discuss and shape up the products to be ready for licensing. We invite all members and also

attendees for US BIO 2018 to participate this session.

These diverse sessions are carefully coordinated to accelerate attendees’ understanding on topics of biotechnology

and pharmaceutical research, industry-academia cooperation, and business development.

In this meeting, KASBP Fellowship Awards offered with the Sponsors will be presented to young scholars from

graduate to post-doctoral levels who exhibit excellences in their research.

This symposium will also provide an opportunity for members to establish professional networks, and share

information and experience in the pursuit of excellence in drug discovery R&D.

The symposium organizing committee is looking forward to meeting all members and friends associated with

pharmaceutical and biotechnology industry as well as academia.

2017-2018 KASBP President 2018 KASBP Spring Symposium Program Chair

Yun H. Choe, PhD/JD Sean Kim, PhD

2 |P a g e 2 0 1 8 K A S B P F a l l S y m p o s i u m

2017-2018 KASBP OFFICERS

Title Name 한글 이름 Affiliation

President Yun H. Choe 최윤 Lucas & Mercanti

President Designated Sean Kim 김승빈 Blueprint Medicines

1st Vice President K. Stephen Suh 서광순 Hackensack Med Center

Executive Director Peter Seongwon Hong 홍성원 Regeneron

Science Director Hyun-Hee Lee

Hyunsuk Suh

이현희 서현석

Merck

Pfizer

Financial Director Sahee Kim

Adv. Seongwoo Hwang

김사희 황성우

RevHealth, LLC

PTC Therapeutics

Web Director DaeHo Lee

Adv. Cheol K. Cheong

이대호 정철근

Genentech

Membership Director Suktae Choi

Sohyun Aria Rhee

최석태 이소현

Celgene

Celgene

Membership Networking

Director

Claire Jeong

Sandy Suh

정가영 서샌디

GSK

Exeltis USA

Publication and Public

Relations Director Hyunjin Shin 신현진 Takeda

YG Director Diana Dahea You 유다혜 Rutgers University

Legal Director Elizabeth Lee 이엘리자베스 Lucas & Mercanti

Auditor Sung Tae Lim 임성택 Sanofi

NJ Chapter President Youngsun Kim 김영선 Adello Biologics

Boston Chapter President Hyunjin Shin 신현진 Takeda

Connecticut Chapter

President Sung-Kwon Kim 김성권 Alexion

Philadelphia Chapter

President KernHee Chang 장건희 Janssen

San Francisco Chapter

President Sunghoon Ma 마성훈 Exelixis

Washington DC Chapter

President Sang Tae Park 박상태 Macrogen

Councilor Young-Choon Moon 문영춘 PTC Therapeutics

Councilor Hak-Myung Lee 이학명 Shire

Councilor Jae-Hun Kim 김재훈 IFF

Councilor Jae Uk Jeong 정재욱 GSK

Councilor Jong Sung Koh 고종성 Genosco


2018 KASBP Spring Symposium Committee

Committee Chair Members*

Program Committee Sean Kim Peter Seongwon Hong, Jaeuk Jeong,

Sung Kwon Kim, Moonkyoung Um, Hanjo Lim

Registration Committee Sahee Kim Daeho Lee, SoHyun Aria Rhee,

Jiyoung Jamie Park, Sahee Kim

Fellowship Committee Hyun-Hee Lee Hyunsuk Suh, JaeUk Jeong,

Seung Yeol Park, Sean Kim

Grant Committee Hak-Myung Lee Sahee Kim, Yun H. Choe

YG Program Committee Diana Dahea You SeoYoung Lee, Sung Ki Kim, Ricahrd Oh,

SeanKim, Jae Uk Jeong

Website and SNS

Management Committee Daeho Lee Sahee Kim, Sohyun Aria Rhee, Jiyoung Jamie Park

Job Fair Committee Jaha Park Suktae Choi, Moonkyoung Um, Sahee Kim

Vendor Exhibition

Committee Sue Kang Sue Kang, Yun H. Choe

PR Committee Gene Hyunjin Shin Jaeuk Jeong

* Members are listed in a random order.


SYMPOSIUM SCHEDULE AT A GLANCE

June 1 (Friday) June 2 (Saturday)

AM 7 7:30 – 8:45 AM Registration and Breakfast

8:45 – 9:00 AM Opening Remarks 8

9:00 – 10:20 AM Scientific Session A

9

10 10:20 –10:30 AM Coffee Break

10:30 –11:30 AM Scientific Session B

Sponsor Presentation 11

11:30 – 12:30 PM Fellowship Awards and

Presentations

PM 12 12:30 – 12:45 PM Group Photo

1 12:45 – 2:00 PM Lunch and Poster Session

2 2:00 – 3:40 PM Scientific Session C

Sponsor Presentation 3 3:00-5:30 PM

Job Fair

-details will be available at

www.kasbp.org

3:40 –3:50 PM Coffee Break

4 3:55 – 5:10 PM Scientific Session D

5 5:10– 5:20 PM Scientific Session

Closing Remarks 5:30 – 6:30 PM

Registration and Networking 6 5:20 pm ~ 5:30 pm Break

5:30 pm ~ 6:00 pm Dinner

Dinner and Discussion

(registeration required)

6:00 – 9:00 PM

Symposium Closing Remarks

9:00 pm ~ 9:10 pm

6:30 – 7:30 PM

Opening & Congratulatory Remarks and

Dinner

7

8 7:30 – 8:30 PM

Keynote Presentation

8:30 – 9:00 PM

Sponsor Presentation

9 9:00 – 10:30 PM

Networking Session

10:30 – 11:55 PM

YG Networking Session

10


SYMPOSIUM SCHEDULE IN DETAIL

June 1, 2018, Friday

Job Fair (Details will be available at www.kasbp.org)

2:00 pm ~ 5:30 pm Organizer: Jaha PARK & Suktae Choi

- Flexible arrangement is also possible during symposium when requested

Registration & Networking

5:30 pm ~ 6:30 pm Sahee KIM, RevHealth, LLC & Registration Team

Opening & Congratulatory Remarks and Dinner

6:30 pm ~ 7:30 pm Moderator: Science Director, Hyun-Hee Lee, Merck

Opening Remark KASBP President: Yun H. Choe, Lucas & Mercanti, LLP

Congratulatory Remarks EunChul Huh (GC Pharma, President)

K. Stephen Suh (KSEA, President Elect)

Toast and Dinner

Keynote Lecture

7:30 pm ~ 8:30 pm Keynote Lecture

Searching for rare mutations in the genome

Peter J. Park, Harvard Medical School, Cambridge, MA, USA

Sponsor Presentation-1 - Hanmi

8:30 pm ~ 9:00 pm Young-Mi Lee, Executive Director, Head of Global External R&D Innovation

Networking Program / Group Networking KASBP-Boston Chapter, Hyunjin Shin, Takeda

9:00 pm ~ 10:30 pm

• Biology

A. Immuno-oncology/Autoimmune/Inflammatory

Moderator: Sung-Kwon Kim

B. Respiratory/Metabolic/Cardiovascular/Aging/Mental/Neurogenerative

Moderator: Kern Chang

C. Cell and Gene Therapy/Viral infection/Rare disease

Moderator: Seunghee Jo

• Chemistry

Moderator: Min-Kyu CHO

• PK/PD/pre-clinical/Clinical Science:

Moderator: Peter Seongwon HONG


• BD/Legal/VC:

Moderators: Jongmin John Kim

• Pharmacy:

Moderator: Sahee Kim

Young Generation (YG) group Discussion Moderator: Dahea You

10:30 pm ~


June 2, 2018, Saturday

Registration & Breakfast 7:30 am ~ 8:45 am

Opening Remarks

8:45 am ~ 9:00 am Moderator: Executive Director, Peter Seongwon Hong, Regeneron

Session A KASBP-CT Chapter President, Sung Kwon KIM, Alexion

9:00 am ~ 10:20 am

• A-1: Success and challenges in therapeutic ADC development

Byong-Chul Lee, 23andMe

• A-2: The discovery of Kisqali® (ribociclib, LEE011), a CDK4/6 inhibitor for the treatment of breast

cancer

Mooje Sung, Novartis

Coffee Break

10:20 am ~ 10:30 am

Session B KASBP-NJ Chapter President, Youngsun KIM, Adello Biologics

10:30 am ~ 11:30 am

• B-1: Quantitative Modeling & Simulation Approaches: Driving Critical Decisions from Research

through Clinical Trials

Jennifer Park, Applied BioMath

• B-2: Sponsor Presentation-2, GC Pharma

Fellowship Award Ceremony Hyun-Hee Lee, Merck

11:30 am ~ 12:30 pm

Photo time

12:30 pm ~ 12:45 pm

Lunch & Poster Presentation

12:45 pm ~ 2:00 pm

Session C KASBP-Phila Chapter President, Kern Chang, Janssen

2:00 pm ~ 3:40 pm

• C-1: Successful building of game-changing biotech company with innovative science and business

strategy

Sang Hoon Lee, ABL Bio

• C-2: Nutrient sensing pathway as a therapeutic target for healthy aging

Sungwoo Kang, Navitor

• C-3: Sponsor Presentation 3, Qurient, Kiyean NAM, CEO

Coffee Break

3:40 pm ~ 3:50 pm


Session D KASBP-SF Chapter President: Sunghoon MA, Exelixis

3:50 pm ~ 5:10 pm

• D-1: Early Stage Interaction with FDA: How to Prepare a Pre-IND meeting and an Initial IND

Haeyoung Ahn, Ahn Bio Consulting

• D-2: Advances in CAR-T cell therapy

Paul Kwon, Novartis

Scientific Session Closing Remarks

5:10 pm ~ 5:20 pm KASBP President: Yun H. Choe, Lucas & Mercanti, LLP

Break

5:20 pm ~ 5:30 pm

Dinner

5:30 pm ~ 6:00 pm

Dinner & Discussion – Let’s License Out

6:00 pm ~ 9:00 pm – Moderator: KASBP-DC Chapter President, Sang-Tae PARK, Macrogen Clinical Laboratory

Several companies from Korea and US will present their product or services. Similar to the last Fall’s Biotech Start

Up Companies session, we will hold a challenging session to discuss and shape up the products to be ready for

licensing. We invite all members and also attendees for US BIO 2018 to participate this session.

• DD-1: EGFR T790M/C797S inhibitors for Lung Cancer Treatment

Korea Research Institute of Chemical Technology (KRICT) by Kwangho Lee

• DD-2: Strategic Non-Clinical Evaluation for Drug Development: T2B Infrastructure

T2B, National Center for Efficacy Evaluation or Respiratory Disease Product by Kyuhong Lee

• DD-3: CXCR4 heteromer as a drug target for precision cancer therapeutics

GPCR by Dongseung Seen

• DD-4: Convergence technology for liquid biopsy

CURIOSIS by Hoyoung Yun

• DD-5: Simple, Fast and Accurate Point-of-Care Micro Biochip for Disease Detection, Monitoring and

Diagnosis

ABIONICS by Eon Soo LEE

• DD-6: Getting On New Trends in Healthcare

MACROGEN by Sang-Tae Park

Symposium Closing Remarks

9:00 pm ~ 9:10 pm KASBP President: Yun H. Choe, Lucas & Mercanti, LLP

See you all again at the Fall Symposium!!


KEYNOTE LECTURE ABSTRACT

Searching for rare mutations in the genome

Peter J. Park, Ph.D., Harvard Medical School, Cambridge, MA, USA

Biography

Dr. Park is Professor of Biomedical Informatics at Harvard Medical School and the director of its Bioinformatics and

Integrative Genomics Ph.D. program. His group (http://compbio.hms.harvard.edu) specializes in computational and

statistical analysis of high-throughput sequencing data in epigenomics and cancer genomics. Originally trained in

applied mathematics (B.A., Harvard; Ph.D., Caltech), he was introduced to molecular biology and genetics during his

postdoctoral studies in biostatistics. His laboratory has developed several algorithms for genome analysis and has

made major contributions to the Encyclopedia of DNA Elements (ENCODE) and The Cancer Genome Atlas (TCGA)

projects. He is a co-leader of the Cancer Data Sciences Program at Harvard/Dana-Farber Cancer Center and a

member of the Division of Genetics at Brigham and Women's Hospital and the Harvard Stem Cell Institute. He is a

recipient of the Sloan Research Fellowship and the Harvard Medical School Young Mentor Award.

Abstract

Each life begins with a single cell sheltering a single genome. But somatic mutations occur over the course of

development due to imperfections in DNA replication and other mutagenic sources, giving rise to each cell having

its unique genome. Recent evidence suggests that such somatic mutations may be responsible for a diverse range

of clinical disorders including neurological ones. I will describe some of our efforts in characterizing somatic

mutations, including our recent work in detection of rare mutations in single neurons using whole-genome

sequencing.

SCIENTIFIC SESSION – SPEAKERS BIO AND ABSTRACTS

Session A

A-1: Success and challenges in therapeutic ADC development

Byong-Chul Lee, 23andMe

Biography

Scientist II, 2016-present, 23andMe, Inc., Antibody development and Head of analytics

Scientist, 2010-2016, Genentech, Inc., ADC technology development

Post-Doc, 2006-2010, Lawrence Berkeley National Lab., Protein engineering

PhD, 2001-2006, UCSF, Biophysics, Solid-phase chemistry and Protein-mimetics

MS, 1997-1999, KAIST, Biological Sciences

BS, 1991-1997, Seoul National University, Biology

Abstract

Antibody-drug conjugates (ADCs) has emerged as one of promising therapeutic modalities for oncology. Kadcyla and

Adcetris are two recently FDA-approved ADCs. The approval of these ADCs has drawn significant attention and many

ADCs are now being tested in pre-clinical and clinical phases with new target antibodies, linkers and payloads. Here

I would like to present a success story about developing next generation anti-target X ADC, and hurdles that we


often encounter during therapeutic ADC development.

A-2: The discovery of Kisqali® (ribociclib, LEE011), a CDK4/6 inhibitor for the treatment of breast cancer

Mooje Sung, Novartis

Biography

Dr. Sung is an Investigator III in Global Discovery Chemistry at Novartis Institute of BioMedical Research. He was a

co-inventor of the cyclin-dependent kinase 4/6, Kisqali. He joined Novartis in 2004 after postdoctoral training at

Harvard University (Prof. Yoshito Kishi). Dr. Sung received a Ph.D. in organic chemistry at the University of

Alabama (Prof. Jin K. Cha). In Korea, he had worked at Daewoong Pharmaceutical Co. for 6 years after he graduated

from Sogang University (MS, 1990) and Korea University (BS, 1988).

Abstract

CDK4/6 is a genetically validated target for the treatment of many types of cancer. Herein we describe approaches

to the identification of inhibitors of CDK4/6 culminating in the discovery of LEE011, which is, to date, the most

selective inhibitor know. Preclinical and clinical single agent and combination studies are shown. LEE011 is currently

in multiple clinical trials including a Phase III registration trial in advanced ER +ve breast cancer patients.

Session B

B-1: Quantitative Modeling & Simulation Approaches: Driving Critical Decisions from Research through Clinical

Trials

Jennifer Park, Applied Biomath

Biography

Jennifer Park is Associate Director of Business Development at Applied BioMath, a company that uses mathematical

modeling and simulation to provide quantitative and predictive guidance to pharma and biotech to help accelerate

and de-risk drug research and development. Jennifer has a BS in Bioengineering from Cornell University and PhD in

Bioengineering and stem cell mechanotransduction from University of California, Berkeley. She has ten years of

experience consulting with pharma and biotech to provide molecular and pharmacological insights to their data.

Prior to Applied BioMath, Jennifer was Associate Research Director at Selventa where she oversaw scientific

collaborations with industry clients in immunology, cancer and respiratory diseases. She used computational biology

approaches to analyze 'omics data for biomarker identification to support patient stratification, identify molecular

subtypes, and develop molecular network models of disease. Prior to Selventa, Jennifer was a scientist at Advanced

Cell Technology (now Astellas) researching stem cell differentiation to red blood cells. At Applied BioMath, Jennifer

engages with potential biotech and pharma partners to discuss how they can use mechanistic PK/PD modeling to

help optimize their drugs parameters and dosing

Abstract

A quantitative systems pharmacology (QSP) model delivered biological insights that demonstrated a weaker binding

molecule is a better molecule than the competitor's tighter binder, helping to inform the decision to accelerate

instead of discard an immuno-modulatory molecule that is now positioned to be best-in-class. During the Phase 1

interim analysis, the QSP model was updated with Phase 1 data to explain non-linear PK and subcutaneous dosing

variability and recommend higher dosing that would inhibit the target in most patients, prompting a change in the


clinical protocol

Session C

C-1: Successful building of game-changing biotech company with innovative science and business strategy

Sang Hoon Lee, ABL Bio

Biography

1982-1987 Seoul National University Biology Education B.S

1987-1989 Seoul National University Developmental Biology M.S

1989-1994 The Ohio State University Molecular, Cellular & Developmental Biology Ph.D

1994-1997 Harvard Medical School & Beth Israel Deaconess Cancer Biology & Angiogenesis

Postdoc

1997-1998 University of California at San Francisco (UCSF) and Gladstone Institute Cancer Biology

Postdoc

1998-2000 Stanford Medical School Cancer Biology & Angiogenesis Scientist (Instructor)

2000-2004 Chiron (Currently Novartis) Cancer Pharmacology and Biomarkers Principal Scientist

2004-2005 AstraZeneca R&D Boston Cancer Biology Principal Scientist

2005-2008 Genentech Oncology Biomarkers Group Leader

2008-2009 Exelixis Molecular& Cellular Pharmacology Senior Scientist

2009-2013 PharmAbcine Co-founder Executive VP & CSO

2013-2016 Hanwha Chemical Bio Head of Bio Senior VP

2016-Present ABL Bio Founder CEO

Abstract

ABL Bio Inc. is a privately held South Korean immuno-oncology and neurodegenerative disease biotechnology

research company founded in 2016. The company uses two platform technologies: bispecific antibodies (BsAbs) that

bind two different antigens of interest, and antibody–drug conjugates (ADCs) that deliver small-molecule drugs to

specific cells. ABL’s most advanced asset is ABL001, a BsAb targeting vascular endothelial growth factor and DLL4

that is in development for the treatment of solid tumors. The product is entering a phase 1 trial, a first for a BsAb in

South Korea. On the ADC front, ABL has partnered with LegoChem Biosciences to codevelop cancer therapeutics

with high linker stability and efficient payload release. Immune check points have become the major cancer

therapies as powerful and promising strategy to stimulate antitumor T cell activity. Bispecific antibodies (BsAbs) are

an alternative option for the treatment of certain types of cancer. These BsAbs are composed of parts of two

different monoclonal antibodies, allowing for dual binding and specificity to two different antigens. ABL Bio is

developing novel bispecific antibody, which can redirect effector T cells for the targeted killing of tumor cells. ABL

Bio’s BsAb binds to target antigen on tumor cells in tumor microenvironment and stimulate signal on T cells by

inducing INF-gamma. The present study shows that BsAb can induce T-cell activation and proliferation in the

presence of target tumor cells, redirect potent T-cell mediated killing of target tumor cells in vitro In the

neurodegenerative disorder space, the company’s latest R&D program, ABL is harnessing its BsAb expertise to

develop next-generation BsAbs designed to maximize blood–brain barrier (BBB) penetrance and therapeutic efficacy.

ABL has developed BsAbs equipped with a potent BBB-penetrating moiety and a disease-targeting moiety that can

be applied to various central nervous system (CNS) diseases. The most advanced molecule is ABL301, an α-synuclein

(SNCA)-targeting BsAb that penetrates the BBB via a receptor-mediated transcytosis (RMT) receptor and is in

development for Parkinson’s disease (PD). ABL Bio’s first-in-class bispecific antibodies for Parkinson’s disease


combine unprecedented blood–brain barrier penetration with a robust mechanism of action for improved

therapeutic efficacy.

C-2: Nutrient sensing pathway as a therapeutic target for healthy aging

Sungwoo Kang, Navitor

Biography

PROFESSIONAL EXPERIENCE

2013-present Founding Scientist, Navitor Pharmaceuticals, Cambridge, MA

EDUCATION AND TRAINING

2006-2013 Postdoctoral, Whitehead Institute for Biomedical Research, Cambridge, MA

Advisor: David M. Sabatini, M.D., Ph.D.

2000-2005 Ph.D., Biophysics, Cornell University, Ithaca, NY

Advisor: Brian R. Crane, Ph.D..

Abstract

Humanity’s lasting dream is to reverse or, at least, postpone aging. In recent years, increasing attention has been

devoted to anti-aging therapies. Existing anti-aging strategies, which aim to slow the aging process and to delay the

onset of age-related diseases, focus on nutrient sensing pathways as therapeutic targets. A leading target for such

interventions is the nutrient response pathway defined by the mechanistic Target of Rapamycin Complex 1

(mTORC1). Inhibition of this pathway extends lifespan in model organisms and confers protection against a growing

list of age-related pathologies. Rapamycin, a known allosteric inhibitor of mTORC1, has drawn considerable attention

in the last few years not only because of its accepted clinical uses in cancer treatment and organ transplantation,

but also for its capacity to prolong life span in multiple model organisms. To this end, Navitor Pharmaceuticals

developed a small molecule (NR1) that binds the small G-protein Rheb and selectively blocks mTORC1 signaling.

Rheb activates mTORC1 in response to nutrient and growth factor signals. NR1 potently inhibits mTORC1 driven

phosphorylation of ribosomal protein S6 kinase beta-1 (S6K1) but does not inhibit phosphorylation of Akt or ERK. In

contrast to rapamycin, NR1 does not cause inhibition of mTOR Complex 2 (mTORC2) upon prolonged treatment.

Furthermore, NR1 potently and selectively inhibits mTORC1 in mouse kidney and muscle in vivo. The data presented

herein suggest that pharmacological inhibition of Rheb is an effective approach for selective inhibition of mTORC1

with therapeutic potential.

Session D

D-1: Early Stage Interaction with FDA: How to Prepare a Pre-IND meeting and an Initial IND

Haeyoung Ahn, Ahn Bio Consulting

Biography

Dr. Hae-Young Ahn is the chief executive officer and president of AhnBio Consulting (ABC), Inc. She is the principal

consultant as well and her expertise is on building drug development strategies and regulatory strategies. Prior to

founding the ABC, she was the deputy director in Division of Clinical Pharmacology 3, Office of Clinical Pharmacology,

Center for Drug Evaluation and Research (CDER), Food and Drug Administration (FDA). She received her B.S. in

pharmacy from Ewha Women’s University, M.S. in pharmaceutics from Seoul National University, and Ph.D. in


pharmaceutics from West Virginia University. She also received a postdoctoral training in pharmaceutics at the

University of Michigan.

Abstract

New drug development is a high-risk, expensive and long-term endeavor: it takes an average of 10 to 15 years and

average cost to develop a new drug has become to exceed more than $2.5 billion. However, when drug

development succeeds, it will give high return.

Successful drug development requires thorough early strategic planning and efficient interactions with regulatory

agencies. Goals of drug development are to provide safe and effective drugs to patients in need, and provide an

appropriate information needed for pharmacotherapy for drug, patients and dose. It is critical for successful drug

development that drug development needs to begin with the goals in mind throughout drug development process,

and drug development as well as regulatory strategies should be planned and executed accordingly. In addition,

before drug companies invest significant amounts of time and resources in developing a new drug product, it is

important that they seek input from regulatory agencies to get guidance on CMC, pre-clinical and clinical strategies

and to cultivate a target product profile early in the development process

In this presentation, a pre-IND meeting and an initial IND will be discussed. Specifically, benefits of having a pre-

IND meeting and how to conduct a pre-IND meeting will be focused on. In addition, an initial IND submission and

a study design of a first-in-human study will be discussed

D-2: Advances in CAR-T cell therapy

Paul Kwon, Novartis

Biography:

- Graduated Bucknell Univ and attended Vanderbilt Univ for grad school.

- Joined Sandoz in 1995 and post the Sandoz-Ciba merger was the biologist for the Novartis HDAC inhibitor

program.

- Took LAQ824 and LBH589 (Farydak (Panobinostat)) through preclinical and early clinical development.

Farydak was approved in Feb 2015.

- Joined the Oncology project, portfolio, strategy management group post initiation of the Panobinostat Ph1

trials and worked on small molecule management as well as most of the Novartis Oncology large molecule pipeline.

- Currently, continuing to manage the IO/ONC preclinical and early clinical large molecule portfolio including

CARTs.

Abstract

Not available

Dinner & Discussion Session

DD-1: KRICT (Korea Research Institute of Chemical Technology)

EGFR T790M/C797S inhibitors for Lung Cancer Treatment

Kwangho Lee

Biography

EXPERIENCE/RESPONSIBILITY


2012- Current Translational Research Institute of Novel Drug (TREND)

Director (미래부 기초연계중개연구 과제책임자)

2012- Current Korea University of Science & Technology

Adjunct Professor (Medicinal Chemistry & Pharmacology)

2011- Current Korea Research Institute of Chemical Technology

Principal Investigator Drug & Bio Research Division

2008- 2011 Avila Therapeutics (merged to Celgene)

Program Team Head (Principal Scientist) Platform study and Oncology area research. covalent inhibition on specific

ligand binding. Inhibitors of Apoptosis (IAP), Epithermal Growth Factor Receptor (EGFR) Mutant Selective Inhibitors

(EMSI), Bruton’s Tyrosine Kinase (BTK) inhibitors for RA and Oncology.

2003- 2008 Novartis Institutes for BioMedical Research, Inc.

Research Investigator I - II Infectious Disease area research (Peptide Deformylase Inhibitors (PDF), Undecaprenyl

Pyrophosphate Synthase Inhibitors (UPPS), HCV NS3/4A protease inhibitors, Elongation Factor Tu inhibitors (EFTU)

and Bacteria Growth Inhibition (BGI): Phenotypic Antibacterial Screening).

1992-1997 CJ Co., Kyunggi-do, Korea

Senior Research Associate Five and a half years pharmaceutical experience in new drug study on antibacterial drugs

(2-Oxazolidinones, Quinolones, and Cephalosporines).

EDUCATION

Harvard University, Postdoctoral Fellow, June 2001 - March 2003

The University of Alabama, Ph D. Organic Chemistry, August 1997 - May 2001

Seoul National University, M.S. Organic Chemistry, March 1990 - February 1992

Seoul National University, B.S. Chemistry, March 1986 - February 1990.

Abstract

Erlotinib (Tarceva) & Gefitinib (Iressa) are currently in clinic use as epidermal growth factor receptor (EGFR) kinase

inhibitors for non-small-cell lung cancer (NSCLC). However, their clinical efficacy is limited by both their mechanism-

based toxicity and the development of drug-resistance mutations, including the gatekeeper T790M mutation.

Afatinib, a quinazoline-based irreversible pan-EGFR inhibitor dubbed as second generation EGFR TKI, is limited in

wide clinical use due to unwanted adverse effect such as severe rash and diarrhea. Osimertinib is a pyrimidine-based

irreversible third generation EGFR-TKI and features selective EGFR T790M inhibition while sparing wild-type EGFR

activity. However, during osimertinib clinical study, various acquired resistances were reported. In particular, polar

nucleophilic cysteine mutation into polar non-nucleophilic serine at EGFR 797 position was detected in resistant

patients. To address newly identified EGFR T790M/C797S mutants, new strategic approach is attempted. In this

presentation, strategy for EGFR catalytic site & allosteric inhibitors and current research progress will be discussed.

DD-2: T2B, National Center for Efficacy Evaluation of Respiratory Disease Product

Strategic Non-Clinical Evaluation for Drug Development: T2B Infrastructure

Kyuhong Lee

Biography

Academic Career

2004 Konkuk University, Republic of Korea PhD in Condensed matter physics

1999 Konkuk University, Republic of Korea MS in Condensed matter physics

1997 Konkuk University, Republic of Korea BS in Physics


Professional Experience

2016-present Head National Center for Efficacy evaluation of Respiratory

Disease product (NCER)

2011-present Head Inhalation Toxicology Research Center, KIT

2015-present Professor Human and Environmental Toxicology, UST

2015-present Associate Editor Molecular and Cellular Toxicology

2016-present Chairperson Education and Certification Committee

2014-2015 Chairperson Planning Committee, Korea Society of Toxicology

2012-2013 Chairperson Academic Committee, Korea Society of Toxicology

2012-present Chairperson Cooperation and Coordination Committee, KoEHS

2011–2014 Associate Professor Pharmacology and Toxicology, UST

2008–2011 Assistant Professor Pharmacology and Toxicology, UST

2008–2010 Senior Scientist Center of Inhalation Toxicology, KIT

2005–2008 Postdoctoral Researcher MRI Team, Korea Basic Science Institute, Korea.

Abstract

T2B (Technology to Business) Infrastructure Center is a consortium of 7 preclinical efficacy evaluation centers

specialized in each disease including (1) cancer, (2) cardiovascular disease, (3) metabolic disease, (4) digestive

disorder, (5) respiratory disease, (6) ocular disease, and (7) arthritis/ immune disease, designated by the Ministry of

Health and Welfare in Korea. We provide reliable "one-stop total solution" service through efficacy evaluation and

clinical consultation and also develop customized/ specialized disease models.

DD-3: GPCR

CXCR4 heteromer as a drug target for precision cancer therapeutics

Dongseung Seen

Biography

Seen, DongSeung, Ph.D., is the founder and CEO of GPCR Therapeutics Inc. since 2013 and before then, he served

as a managing director at Macrogen. Previously, he worked at Neurogenex(later Newgex) from 2001 to 2012 and

led M&A with Boram Pharm. Co., Inc. as a CEO. Earlier in his career, he worked as a biotech researcher at LG Chemical.

Dr. Seen earned his BS, MS and Ph.D. from Seoul National University.

Abstract

Chemokine receptor 4 (CXCR4) plays pivotal roles in the proliferation, survival, and invasiveness of cancer cells.

Various anti-cancer drugs targeting CXCR4 has been developed from AMD-3100, but that is an ongoing challenge.

To avoid potential side effects associated with conventional CXCR4 antagonists and to develop more efficient anti-

cancer drugs targeting CXCR4, new paradigm is required. CXCR4 forms heteromers with different GPCRs. There exists

a need for identifying functional GPCR heteromers, such as CXCR4-GPCRx, and developing their inhibitors for use as

GPCR heteromer-targeting cancer therapeutics with higher efficacy and lower side effects. GPCR therapetics Inc.

was founded to develop CXCR4 heteromer inhibitors. For the development of CXCR4 inhibitors, GPCR therapeutics

and Samsung medical center have been collaborating in patient derived xenograft and antibody discovery. Up to

now, GPCR therapeutics Inc. fund-raised about 12 million dollars from 7 Venture capitals. Now, 26 persons work for

GPCR therapeutics Inc.


DD-4: CURIOSIS

Convergence technology for liquid biopsy

Hoyoung Yun

Biography

2015 - present CURIOSIS, INC.

Founder and CEO

Seoul, Korea

2014 - present ENVISIBLE, INC.

Co-founder and COO

Seoul, Korea

2013 - Present Cytoneers, Inc.

Founder and CEO Rochester, MI

November 2011

- January 2013

Postdoctoral Research Fellow, Harvard University Cambridge, MA

- Rowland Institute at Harvard

March 2011

- May 2011

Postdoctoral Research Fellow, Seoul National University Seoul, Korea

- Multiscale Biomedical Engineering Laboratory (Advisor: Prof. Noo Li Jeon)

September 2010

- February 2011

Research Assistant, Seoul National University Seoul,, Korea

- New Media Laboratory (Advisor: Prof. Hyunwoo Bang)

March 2005

- August 2010

Research Assiatant, Seoul National University Seoul, Korea

- Advanced Machine Element Design Laboratory (Advisor: Prof. Dong-Chul Han)

January 2004

- February 2005

Researcher, NanoEntek Inc. [KOSDAQ 039860] - Former Digital Bio Technology Co.

Seoul, Korea

EDUCATION

March 2005

- February 2011

SEOUL NATIONAL UNIVERSITY Seoul, Korea

Ph.D. in Mechanical & Aerospace Engineering

- Thesis: A Microchip flow cytometer for multiplexed immunoassays using fluorescent

nanoparticles - Completed an integrated M.S.-Ph.D. course in Mechanical Engineering - Advisor: Prof. Dong-Chul Han and Prof. Hyunwoo Bang

March 1999

- February 2004

HANYANG UNIVERSITY Seoul, Korea

B.S. in Mechanical Engineering

.

Abstract

Human body has a treatment system that automatically identifies and analyzes the cause of external attack. It is

called an immune reaction through an antigen-antibody reaction. The immune system of human body has an

almost perfect defense system covering most risk factors from a tiny scratch to a serious infectious disease. A great

number of researchers all over the world are proceeding research on the principle of human body’s immune system

since revealing the precise mechanism of the immune system leads to solving representative conundrum of modern

medicine such as infection, tissue regeneration, stem cell therapy, and organ transplant. Nonetheless, the current

experiment method takes a lot of time, and does not exactly reflect the actual human immune system because at

most time laboratory animals are used. The existing immunoassay equipment requires a mess of cell, antibody, and


protein and needs three to five days of diagnosis time. Moreover, it has both inefficiency and large standard errors

due to the absence of an automatic system. To overcome such weaknesses, our project aims at (1) developing and

producing microfluidics that is appropriate for immunoassay system as well as is available for mass production, (2)

designing a system where all the procedure from specimen preprocessing to cell culture can be automatically

embodied, (3) developing a new analysis system which enables a high speed, high-sensitive screening based on a

fluorescence analysis, not based on a simple microscopic imaging analysis.

DD-5: ABONICS

Simple, Fast and Accurate Point-of-Care Micro Biochip for Disease Detection, Monitoring and Diagnosis

Eon Soo LEE

Biography

Dr. Eon Soo Lee is Founder of ABONICS, INC which is a newly established startup for the biochip technology for

disease detection, diagnosis and monitoring. The biochip technology has been developed for many years by Dr. Lee’s

research group since his joining as Assistant Professor in Mechanical Engineering at New Jersey Institute of

Technology (NJIT) in 2013, and has received many national and international recognitions including New Jersey

Health Foundation, NIH and IEEE-EMBS society, National Science Foundation, and TechConnect Conference. He has

been serving as Director of Advanced Energy Systems and Microdevices Laboratory- a translational academic

research laboratory dedicated to the energy and microdevices technologies including biomedical device researches.

He has extensive research experiences on small scale flow dynamics and bio-agent reactions in both academia and

industries including Stanford University and NJIT, and Samsung R&D Center as a Principal Research Engineer, where

Dr. Lee was awarded a prestigious Samsung Technology Award in 2011 by the significant achievement of the

technology development. He has received his PHD (2007) and MS (2004) in Mechanical Engineering at Stanford

University, and his BS (1999) in Mechanical Engineering at Yonsei University, Seoul, Korea.

Abstract

Complex disease detection like ovarian cancer cannot be performed at the physician’s office due to the technological

limitations in the current diagnosis process with respect to the sample preparation, sample volume, limit of

detection and duration of analysis. The simple, inexpensive and highly accurate micro biochip device using real-

time quantitative measurements of disease biomarkers from a finger prick blood sample significantly minimize the

complexities in current diagnosis processes as shown in Figure-1 (Patent filed: PCT/2017/038554). The biochip

invention has a very novel approach in the following technical aspects: (1) Self-separation of blood plasma from the

whole blood is involved in the diagnostic process that helps in minimizing the contamination of the sample and

significantly reduce the time and effort of the diagnosis process for blood separation. (2) Detection of multiple

biomarkers with different concentration levels from a single test and easily expandable sensing platform to detect

different biomarkers. (3) Detection of the biomarker in pico and sub-pico level concentration using the nano scale

electrodes in the sensing mechanism as shown in Figure-1. (4) Generation of instantaneous results using the

electrical sensing mechanism.


DD-6: MACROGEN

Getting On New Trends in Healthcare

Sang-Tae Park

Biography

EDUCATION Ph.D in Molecular Microbiology, Yonsei University, Seoul, Republic of Korea, Feb 2004 M.S. in Microbiology, Yonsei University, Seoul, Republic of Korea, Feb 1998 B.S. in Biology, Yonsei University, Seoul, Republic of Korea, Feb 1996

EXPERIENCES

Macrogen Corporation, Rockville, MD

- CEO/CSO, 2014 - present

Macrogen Corporation (“Macrogen Clinical Laboratory” & “Axeq Technologies”), Rockville, MD

- CEO, 2014

Macrogen Clinical Laboratory, Rockville, MD

- GM (Director of Lab Operation), Clinical Business Department. 2012 - 2013

TB Systems Biology Program (The Broad Institute of MIT and Harvard, National Emerging Infectious Diseases

Laboratories, and Biomedical Engineering at Boston University), Boston, MA

- Research Associate Scientist with Dr. James E. Galagan, 2009 – 2012

Harvard Medical School/Children’s Hospital, Boston, MA

- Research Fellow with Robert N. Husson, 2004 – 2009.

Abstract

Macrogen Corp. (Rockville, MD), established in 2005, also shares two decades of experience of Macrogen Inc. (Seoul,

Korea) in top-quality genomic sequencing. With its origins of Korea, Macrogen is continually expanding both globally

and with the services that it provides, including the launching of CLIA-certified services in 2012. In 2018, Macrogen

is one of the Top 10 Sequencing Companies according to recent report from Clinical Omics.

Macrogen strives to get on new trends in healthcare market from research based sequencing market including

Sanger sequencing and Next-Generation sequencing services. Every countries have own regulation with their

concerns and systems and the U.S. is the well-regulated and leading country with licenses and regulations for clinical

diagnostics in the world. Macrogen Corp. has been acquiring licenses to expand to clinical market with eligible

clinical services from the research based service market. Now, Macrogen Corp. has licenses from 50 states in the U.

S. and CAP for human genomic diagnostic fields. Macrogen Corp. has been participating and completing in many of

genome sequencing projects in the U.S. such as TOPMed by NIH/NHLBI and Parkinson’s diseases project by NIH/NIA.

So far, Macrogen Corp. has been providing about 40,000 WGS results to public databases directly and indirectly.

Also, Macrogen is the one of founders in GA100K (GenomeAsia 100K) for accelerating Asian population specific

medical advances and precision medicine. Along with leading this GA100K project, Macrogen is trying to building

the Asian specific reference genome data with various genomic and medical information for providing proper

reference genome in Asian genome studies. Macrogen will continue efforts to get on new trends in the new

healthcare market with adapting new technologies as well as following regulations in the market to fulfill the vision

of personalized medicine, “Humanizing Genomics”.


POSTER SESSION – AWARDEE ABSTRACTS

2018 SPRING FELLOWSHIP AWARDEES

KASBP - YUHAN

Sangdoo Kim, Ph.D. Harvard Medical School

Baehyun Shin, Ph.D. Harvard Medical School

Mikyung Yu, Ph.D. Harvard Medical School

KASBP - GREEN CROSS

Jae Yeon Hwang, Ph.D. Yale University

Youngjin Kim, Ph.D. Rockefeller University

KASBP - HANMI

Seungkyu Lee, Ph.D. Harvard Medical School

Yeong Shin Yim, Ph.D. MIT

Dahea Yu Rutgers

KASBP - QURIENT

Soeun Kang University of Illinois at Chicago

Do Hyung Kim, Ph.D. Johns Hopkins University

P-1: The presence of Th17 cell-inducing bacteria in the maternal gut promote autism-like phenotype in

offspring

Sangdoo Kim1*, Hyunju Kim1*, Yeong Shin Yim2, Soyoung Ha1, Koji Atarashi3, Tze Guan Tan4, Randy S. Longman5,

Kenya Honda3, Dan R. Littman6,7, Gloria B. Choi2 & Jun R. Huh1† 1Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston,

Massachusetts 02115, USA, 2The McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences,

Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA, 3Department of Microbiology and

Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan, 4Department of Microbiology and

Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA, 5The Jill Roberts Institute for Research

in IBD, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, New York, New York 10021, USA, 6The

Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York,

New York 10016, USA, 7Howard Hughes Medical Institute, New York, New York 10016, USA, †Present address: Division

of Immunology, Department of Microbiology and Immunobiology and Evergrande Center for Immunological

Diseases, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts 02115, USA, *These

authors contributed equally to this work.

Several epidemiological studies have suggested that viral infection of women during pregnancy correlates with an

increased frequency of autism spectrum disorder (ASD) in children. In the rodent maternal immune activation (MIA)

model of this phenomenon, offspring from pregnant mice injected with poly(I:C), a mimic of viral infection, exhibit

behavioral abnormalities as well as cortical abnormalities in offspring. Previously we demonstrated that interleukin-


17a (IL-17a) produced by T helper 17 (Th17) cells in pregnant mothers promotes behavioral and cortical

abnormalities in the offspring exposed to MIA. However, it is unclear whether other maternal factors are required

to promote MIA-associated phenotypes. Moreover, the underlying mechanisms by which MIA leads to T cell

activation with increased IL-17a in the maternal circulation are not well understood. In this study, we show that

MIA phenotypes in offspring require maternal intestinal bacteria that promote Th17 cell differentiation. For

example, pregnant mice that had been colonized with mouse commensal segmented filamentous bacteria (SFB) or

human commensal bacteria that induce Th17 cells are more likely to produce offspring with MIA-associated

phenotypes. Overall, our data suggest that gut microbial communities in women during pregnancy that promote

excessive Th17 cell differentiation may be more likely to bear children with autistic spectrum disorder in the event

of uncontrolled inflammation.

P-2: Novel DNA aptamers that bind to mutant huntingtin and modify its activity

Baehyun Shin1, 2, Roy Jung1, 2, Hyejin Oh1, 2, Gwen E. Owens3, Hyeongseok Lee4, Seung Kwak5 , Ramee Lee5, Susan L.

Cotman1, 2, Jong-Min Lee1, 2, Marcy E. MacDonald1, 2, Ji-Joon Song4, Ravi Vijayvargia1, 2 and Ihn Sik Seong1, 2

1Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA, 2Department of Neurology,

Harvard Medical School, Boston, MA 02114, USA, 3Division of Biology and Biological Engineering, California Institute

of Technology, Pasadena, CA, USA, 4Department of Biological Sciences, Center for Cancer Metastasis, Korea

Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea, 5CHDI Foundation,

Princeton, NJ 08540, USA

Purpose: The CAG repeat expansion that elongates the polyglutamine tract in huntingtin is the root genetic cause

of Huntington’s Disease (HD), a debilitating neurodegenerative disorder. We found its polyglutamine tract size

influences both huntingtin’s structure and function, including modulating its activity in stimulating polycomb

repressive complex 2 (PRC2). These observations strongly imply that small molecules that preferentially bind to

mutant rather than normal huntingtin can be found and that, in doing so they may selectively influence the impact

of the longer polyglutamine tract on mutant huntingtin activity.

Materials & Methods: To provide an initial proof for the concept of small molecule-binding as a route to directly

alter the impact of the expanded polyglutamine tract on mutant huntingtin, we have screened a library of single

stranded DNA aptamers for mutant huntingtin specific binders, using highly purified human recombinant huntingtin

with polyglutamine tract lengths of either 23- or 78-residues. This biochemical strategy has yielded a specific set of

aptamers that exhibit differential binding affinities to mutant and normal huntingtin. In this study, we have evaluated

the aptamers’ binding sites and potential ability to modulate the effects of polyglutamine tract length on huntingtin

structure, PRC2-stimulating activity and therapeutic effects in HD human neural progenitor cells (hNPC).

Results: We identified forty-five DNA aptamers that preferentially bind to Q78-huntingtin compared to Q23-

huntingtin. One of top aptamers, MS3, was chosen for further validation. First, MS3 showed the same or similar

strong affinity to Q46-huntingtin, indicating our DNA-aptamer can be utilized for adult-onset CAG range (below Q50)

as well as juvenile-onset CAG range (i.e. Q78). Moreover, we found that MS3 binds mutant huntingtin proximal to

lysines K2932/K2934 in the carboxyl-terminal CTD-II domain. When we tested a functional effect of aptamer binding,

aptamer-bound mutant huntingtin abrogated the enhanced PRC2 stimulatory-activity conferred by the expanded

polyglutamine tract. In a pull-down assay, the MS3-beads produced a 3.6-fold more efficient pull-down of huntingtin

from HD hNPC (HD60i4) lysate compared to normal hNPC (HD17m8) lysate, although total huntingtin levels in both

cells were similar. Furthermore, in HD hNPC, but not normal hNPC, MS3 aptamer co-localized with endogenous

mutant huntingtin and was associated with significantly decreased PRC2 activity. Moreover, the cellular ATP content

and cell viability in starving condition, which are well known as HD cellular phenotypes by revealing decreased ATP

level and reduced cell viability in starving condition, were significantly increased by MS3 aptamer transfection in HD

hNPC specifically but not by stem-loop DNA oligonucleotides (GCdx). Therefore, DNA aptamers can preferentially


target mutant huntingtin and modulate a gain of function endowed by the elongated polyglutamine segment.

Conclusion & Future study: These mutant huntingtin binding aptamers provide novel molecular tools for delineating

the effects of the HD mutation and encourage mutant huntingtin structure-based approaches to therapeutic

development. We will validate the functional in vivo consequence of DNA aptamers in HdhQ111 CAG knock-in mice,

a precise genetic model of the HTT CAG mutation, expressing full-length mutant HTT via collaboration with Dr.

Wheeler in CGM. These approaches will guide us to develop promising therapeutic molecules as drug candidate for

HD.

Author Contact: Baehyun Shin, Ph.D, [email protected], 617-631-4917

P-3: Targeted Nanotherapeutics Encapsulating Liver X Receptor Agonist GW3965 Enhance Antiatherogenic

Effects without Adverse Effects on Hepatic Lipid Metabolism in Ldlr−/− Mice 1Mikyung Yu, 2Jaume Amengual, 2Arjun Menon, 1Nazila Kamaly, 2Felix Zhou, 1Xiaoding Xu, 1Phei Er Saw, 3Seung-Joo

Lee, 1Kevin Si, 1Carleena A. Ortega, 1Won Il Choi, 1In-Hyun Lee, 1Yazan Bdour, 1Jinjun Shi, 1Morteza Mahmoudi, 4Sangyong Jon, 2Edward A. Fisher,* and 1Omid C. Farokhzad* 1Center for Nanomedicine and Department of Anesthesiology, Brigham and Women’s Hospital, Harvard Medical

School, Boston, MA 02115, USA, 2Division of Cardiology, Department of Medicine, Marc and Ruti Bell Program in

Vascular Biology, New York University School of Medicine, New York, NY 10016, USA, 3Department of Biological

Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Ave., Boston, MA 02115, USA, 4KAIST Institute for the BioCentury, Department of Biological Sciences, Korea Advanced Institute of Science and

Technology (KAIST), 291 Daehak-ro, Daejeon 34141, Republic of Korea.

The unique roles of liver X receptors (LXRs) as a master regulator of the reverse cholesterol transport pathway in

lipid homeostasis and an anti-inflammatory agent have attracted much attention in the field of drug discovery for

the treatment of atherosclerosis. Unfortunately, pharmacological manipulation of LXRs through LXR agonists has

not received FDA approval due to the undesirable increase in plasma and hepatic levels of lipids such as triglyceride.

To safely activate the LXR pathway, this study presents the development and efficacy of controlled-release

nanoparticles (NPs) incorporating the synthetic LXR agonist GW3965 (GW) for targeted delivery to atherosclerotic

plaques. Collagen IV (Col IV) targeting peptide ligands were employed to functionalize the polymer-lipid based NPs

to improve targeting to the atherosclerotic plaque, and formulation parameters including the length of the

polyethylene glycol (PEG) coating molecules were systematically optimized. In vitro studies indicated that the GW-

encapsulated NPs upregulated the LXR target genes in mouse peritoneal macrophages, whereas they

downregulated proinflammatory mediator. The Col IV-targeted NPs encapsulating GW (Col IV–GW–NPs) successfully

reached advanced atherosclerotic lesions of high fat-fed ldlr-/- mice when administered for 5 weeks and

substantially reduced macrophage content (≈30%) of the atherosclerotic lesion compared to the free GW group

(n=6~8), demonstrating improved antiatherogenic effects. Particularly, the ldlr-/- mice administered the Col IV–GW–

NPs did not increase hepatic lipid biosynthesis or hyperlipidemia during the treatment period, unlike mice injected

with the free GW. Our findings suggest a new form of LXR-based therapeutics capable of enhanced delivery of the

LXR agonist to atherosclerotic lesions without altering hepatic lipid metabolism.

Presenter: Mikyung Yu, PhD (Brigham and Women’s Hospital/Harvard Medical School)

Address: 60 Fenwood Rd., Building for Transformative Medicine (BTM) 7002C, Brigham and Women’s Hospital,

Boston, MA, 02115

Email: [email protected]; Phone number: 617-733-3141

P-4: Efcab9 and CatSper Couple pH and Ca2+ sending of sperm Calcium channel to regulate motility

Jae Yeon Hwang1, Nadja Mannowetz2, Yongdeng Zhang3, Joerg Bewersdorf3, Polina V. Lishko2, and Jean-Ju Chung1,4*


1Department of Cellular and Molecular Physiology, 3Department of Cell Biology, 4Department of Gynecology and

Obstetrics, Yale School of Medicine, New Haven, CT 06510, 2Department of Molecular and Cell Biology, University of

California Berkeley, Berkeley, CA, 94720. *Correspondence: [email protected]

CatSper is the weakly voltage dependent, pH-activated calcium channel in sperm cells, where it mediates Ca2+ entry

required for hyperactivated motility and male fertility. CatSper channels exist as a multi-subunit complex that

organizes linear Ca2+ signaling nanodomains in the flagellar membrane along the sperm tail. However, the

cytoplasmic machinery modulating the channel activity remains poorly understood. We sought to find modulators

of CatSper channel using proteomic and comparative genomic screens and identified a novel EF-hand protein,

EFCAB9. We show that EFCAB9 interacts directly with CatSper that dissociates at elevated pH and Ca2+

concentrations. Studies using knockout mice created by CRISPR/Cas9 show that EFCAB9 in complex with CatSper

confers pH-dependent activation of CatSper channel. In the absence of Efcab9, sperm motility and fertility is

compromised and the linear arrangement of the Ca2+ signaling domains is disrupted. These observations suggest

that EFCAB9 is pH-dependent Ca2+ sensor from the cytoplasmic mouth of CatSper channels and regulates

hyperactivated motility.

Key words: Sperm, CatSper channel, Hyperactivation, pH, and Calcium

E-mail: [email protected]; Cell: 203-654-0657

P-5: Molecular structure of human P-glycoprotein in the ATP-bound, outward-facing conformation

Youngjin Kim and Jue Chen*

Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.

The multidrug transporter permeability (P)-glycoprotein is an adenosine triphosphate (ATP)-binding cassette

exporter responsible for clinical resistance to chemotherapy. P-glycoprotein extrudes toxic molecules and drugs

from cells through ATP-powered conformational changes. Despite decades of effort, only the structures of the

inward-facing conformation of P-glycoprotein are available. Here we present the structure of human P-glycoprotein

in the outward-facing conformation, determined by cryo-electron microscopy (EM) at 3.4-Å resolution. The two

nucleotide-binding domains form a closed dimer occluding two ATP molecules. The drug-binding cavity observed in

the inward-facing structures is re-orientated toward the extracellular space and compressed to preclude substrate

binding. This observation indicates that ATP binding, not hydrolysis, promotes substrate release. The structure

evokes a model in which the dynamic nature of P-glycoprotein enables translocation of a large variety of substrates.

P-6: Characterization of charged N-type voltage-gated Ca2+ channel blockers for targeted synaptic silencing

of nociceptors

Seungkyu Lee1,2, Sebastien Talbot1, Jinbo Lee3, Bruce P. Bean2, and Clifford J. Woolf1,2

1F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA, 2Department of Neurobiology,

Harvard Medical School, Boston, MA 02115, USA, 3Sage Partner International, Andover MA 01810

Email: [email protected] C.P. 617-620-1238

Current pain treatment options are generally unsatisfactory with low efficacy and deleterious side effects. Selective

silencing of nociceptors is a useful strategy to address these unmet needs. We previously showed that QX-314, a

permanently charged lidocaine derivative, went into nociceptors through TRPV1 channel pore and then inhibited

voltage-gated Na+ channels (VGSCs). Internalized QX-314 blocked pain behavior without any motor deficits with a

long duration (Binshtock et al., 2007) and reduced neurogenic inflammation in an asthma model (Talbot et al., 2015).

In this case, the VGSCs that are involved in action potential generation for pain signaling were targeted. However,

targeting voltage-gated Ca2+ channels (VGCCs) in nociceptors will be effective as analgesics and neurogenic


inflammation treatments, if they result in a blockade of synaptic transmission in presynaptic nerve terminals as well

as of peptide release from peripheral nerve endings. To develop novel charged VGCC blockers, we identified neutral

N-type channel blockers (NNCBs) from compound screening and characterized their inhibitions on HEK cells

expressing N-type VGCC and primary sensory neurons. Second, cationic N-type channel blockers (CNCBs) were

synthesized by introducing a quaternary ammonium group. Their effects of the compounds outside and inside of

the cells were tested. These charged inhibitors of VGCCs will be used in selectively silencing synapses in nociceptors

and potentially become analgesics and treatments for neurogenic inflammation with high efficacy and reduced side

effects.

P-7: Reversing behavioral abnormalities in mice exposed to maternal inflammation

Yeong Shin Yim1,2, Ashley Park1,2, Janet Berrios1,2, Mathieu Lafourcade1,2, Leila M. Pascual1,2, Natalie Soares1,2, Joo

Yeon Kim1,2, Sangdoo Kim3, Hyunju Kim3, Ari Waisman4, Dan R. Littman5, 6, Ian R. Wickersham1 , Mark T. Harnett1,2,

Jun R. Huh3, Gloria B. Choi1,2 1McGovern Institute for Brain Research, 2Department of Brain and Cognitive Neuroscience, Massachusetts Institute

of Technology, Cambridge, MA 02139, USA, 3Division of Immunology, Department of Microbiology and

Immunobiology, Harvard Medical School, Boston, MA 02115, USA and Evergrande Center for Immunological

Diseases, Harvard Medical School and Brigham and Women’s Hospital, Boston, MA 02115, USA, 4Institute for

Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany, 5Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York,

NY 10016, USA, 6Howard Hughes Medical Institute, New York, NY 10016, USA.

E-mail address: Yeong Shin Yim ([email protected])

Viral infection during pregnancy is correlated with increased frequency of neurodevelopmental disorders. This

phenomenon has been studied in mice prenatally subjected to maternal immune activation (MIA). We previously

showed that maternal T helper 17 (Th17) cells promote the development of cortical and behavioral abnormalities

in MIA-affected offspring. However, it remains unclear if and how cortical abnormalities serve as causative factors

for the aberrant behavioral phenotypes. Here, we show that cortical abnormalities are preferentially localized to a

region encompassing the dysgranular zone of the primary somatosensory cortex (S1DZ) in the adult MIA offspring

and that the presence and size of cortical patches tightly correlated with manifestation and severity of MIA-

associated behavioral phenotypes. Moreover, activation of pyramidal neurons in this cortical region was sufficient

to induce MIA-associated behavioral phenotypes in wild-type animals, while reduction in neural activity rescued the

behavioral abnormalities in MIA-affected offspring. Furthermore, we identified the temporal association area (TeA)

and the striatum as potential S1DZ downstream targets involved in the selective modulation of sociability and

repetitive behavioral phenotypes, respectively. Our work identifies a cortical region primarily, if not exclusively,

centered on the S1DZ as the major node of a neural network that mediates behavioral abnormalities observed in

offspring exposed to maternal inflammation.

P-8: Epigenetic Regulation of the MDR1 Transporter at the Human Blood-Brain Barrier: Interplay Between

Histone Acetylation and Aryl Hydrocarbon Receptor Signaling

Dahea You1, Xia Wen2,3, Jason R. Richardson4, Lauren M. Aleksunes2,3. 1Joint Graduate Program in Toxicology, Rutgers University, Piscataway, NJ, 2Environmental and Occupational Health

Sciences Institute, Rutgers University, Piscataway, NJ, 3Department of Pharmacology and Toxicology, Rutgers

University, Piscataway, NJ, 4Northeast Ohio Medical University, Rootstown, OH

Multidrug Resistance Protein 1 (MDR1, ABCB1) is a key efflux transporter that extrudes chemicals from the blood-

brain barrier (BBB) and regulates the efficacy and/or toxicity of xenobiotics in the brain. Our previous studies have


indicated that the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) or Zolinza®

significantly up-regulated the expression and the function of MDR1 in immortalized human brain capillary

endothelial (hCMEC/D3) cells, a model of the BBB. In the current study, we sought to identify the mechanism by

which HDAC inhibitors up-regulate the MDR1 transporter. Using a panel of HDAC inhibitors including SAHA, we found

that the up-regulation of MDR1 mRNA by HDAC inhibitors mirrored increases in the mRNA expression of the aryl

hydrocarbon receptor (AHR) (R2=0.9). We investigated the role of AHR in regulating MDR1 in human brain

endothelial cells by testing the effects of β-naphthoflavone (BNF), an AHR activator, and CH-223191 (AHRi), an AHR

inhibitor, during HDAC inhibition. At 6 hr, BNF alone had no effect on MDR1 mRNA expression while SAHA increased

it by 160%. However, concurrent exposure to both BNF and SAHA induced MDR1 mRNA by 290%. mRNA expression

of CYP1A1, a known target of AHR, was also increased to a much greater extent by this combination. At 12 hr, AHRi

did not significantly change the basal level of MDR1 mRNA, but attenuated SAHA-mediated induction of MDR1

mRNA by 60%. Induction of CYP1A1 mRNA by SAHA was also significantly reduced by AHRi. Collectively, these results

suggest that AHR is a potential regulator of MDR1 transporter following HDAC inhibition in human blood-brain

barrier cells.

Funded by R01ES021800, P30ES005022, and a Bristol-Myers Squibb Fellowship.

P-9: Monitoring the Glutathione Redox Reaction in Living Human Cells by Combining Metabolic Labeling with

Heteronuclear NMR

Soeun Kang,[a] Xing Jin,[b] Shinya Tanaka,[c] and Sunghyouk Park*[b]

[a] Department of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago,

Illinois 60607, USA ([email protected], +1-312-366-7919), [b] College of Pharmacy, Seoul National University, 1

Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea, [c] Department of Pathology, Laboratory of Cancer Research, N15, W7,

Kita-ku, Sapporo, 060-8638, Japan

The glutathione (GSH) redox reaction is critical for defense against cellular reactive oxygen species (ROS). However,

direct and real-time monitoring of this reaction in living mammalian cells has been hindered by the lack of a facile

method. Herein, we describe a new approach that exploits the GSH biosynthetic pathway and heteronuclear NMR.

[U-13C]-labeled cysteine was incorporated into GSH in U87 glioblastoma cells, and the oxidation of GSH to GSSG by

a ROSproducing agent could be monitored in living cells. Further application of the approach to cells resistant to

temozolomide (TMZ), an anti-glioblastoma drug, suggested a possible new resistance mechanism involving

neutralization of ROS. This result was corroborated by the observation of up-regulation of glutathione peroxidase 3

(GPx3). This new approach could be easily applied to redox-dependent signaling pathways and drug resistance

involving ROS.

P-10: A non-tight junction function of claudin-7 protein in lung cancer progression

Do Hyung Kim1,2†, Zhe Lu1†, Junming Fan1, Qun Lu1, Kathryn Verbanac1, Lei Ding1, Randall Renegar1 and Yan-Hua

Chen1 1Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA, 2Johns Hopkins School of Medicine,

Baltimore, MD 21287, USA, † Contributed equally

E-mail address: [email protected], Telephone: (847)-946-8314

Claudins are a family of tight junction (TJ) membrane proteins involved in a variety of human diseases including

cancer. Claudin-7 is a unique TJ membrane protein in that it has a strong basolateral membrane distribution in

epithelial cells and in tissues to provide the cell polarity. However, the mechanism of claudin-7 in human cancer

progression has not been well characterized unlike other tight junction proteins. We have found that claudin-7 co-

localizes and formed a protein complex with integrin β1. To study the function of claudin-7, we established the stable


knockdown of claudin-7 expression in human lung cancer cells upon the transduction of lentiviral claudin-7 shRNA

(claudin-7 KD cells). The claudin-7 KD cells reduced integrin β1 and phospho-FAK levels and the cell attachment.

However, the KD cells increased the human lung tumor growth and cell cycle progression. These results suggest the

dual function of claudin-7 in regulating human lung cancer cell progression.

POSTER SESSION –ABSTRACTS

P-11: Total Synthesis of a Bioactive Natural Product Colletochlorin B

Sun A. Choi, Gennadii Grabovyi, Justin T. Mohr

Department of Chemistry (MC 111) - University of Illinois at Chicago, 845 West Taylor Street, Chicago, IL 60607-7061

E-mail: [email protected], Tel: 224-935-0060

Natural sources including plants, fungi, and bacteria produce many secondary metabolites that are also known as

natural products. Some bioactive natural products are developed into pharmaceutical drugs and developing a way

to mass produce bioactive natural products using synthetic chemistry is a critical step in meeting global healthcare

needs. In this project, a bioactive natural product, colletochlorin B, which shows antifungal and anticancer activity

is synthesized from 5-methylcyclohexane-1,3-dione and citral, commercially available compounds. Colletochlorin B

was first discovered from the fungus Colletotrichum nicotianae and the structure of this target compound is a

complicated aromatic system that contains multiple functional groups. Multiple reaction steps were taken to add

each functional group at a specific location of the original compound.

P-12: p38 MAPK functions as a tumor suppressor in skin epithelial cells, but as a tumor promoter in myeloid

cells

Min-Kyung Choo and Jin Mo Park

Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA

02129, USA

[email protected], [email protected]

617-726-4456 (lab) 617-543-5663 (mobile)

The p38 MAP kinase plays a pivotal role in cellular responses to stress, mitogenic stimuli and immune signaling.

Evidence from clinical observations and cell culture experiments reveals a role for p38 in many aspects of cancer

and immunity. Meanwhile, attempts to determine the physiological role of p38 in mice have been hampered due

to the early embryonic lethality of mice null for p38alpha, the most abundant and ubiquitously expressed p38

isoform. To overcome this challenge, we generated conditional knockout mice in which p38alpha expression was

specifically ablated in epithelial cells and immune cells, and have discovered that p38alpha plays a crucial role in

inflammation and immune response in a cell type-dependent manner. Here, we investigated the role of p38alpha

in keratinocytes and myeloid cells in a chemically induced skin carcinogenesis model. Our study using conditional

knockout animals showed that keratinocyte- and myeloid-specific p38α ablation resulted in an increase and

decrease, respectively, in tumor incidence. Furthermore, tumors from the two groups of mutant mice displayed

contrasting histological features in the intratumoral and tumor-stromal areas. Interestingly, tumors derived from

p38alpha-deficient keratinocytes highly expressed p63 positive stem cell populations. Mechanistically, we

discovered that p38alpha directly phosphorylated and thereby destabilized p63. We identified the amino acid

residues on p63 that were directly phosphorylated by p38alpha in vivo and in vitro. p63 phosphorylation by

p38alpha contributed to shaping keratinocyte gene expression related to stem cell homeostasis, inflammation, and

tumorigenesis. These findings illustrate a novel link between stress-induced protein kinase signaling and p63-


dependent epidermal homeostasis. On the other hand, p38 ablation in macrophages upregulated chemokine

expression to recruit cytotoxic T cells to tumor microenvironments and resulted in tumor regression. We found that

LPS-induced expression of ATF3, a transcription factor to negatively regulate T cell-recruiting chemokine, was

reduced in p38alpha-deficient mouse and human macrophages, and p38alpha-overexpression increased ATF3 level.

Therefore, ATF3 may link to p38alpha to chemokine expression in macrophages. These data suggest that p38alpha

in epithelial cells and myeloid cells plays a distinct role in skin tumorigenesis and cell type-specific targeting should

be considered to increase drug efficacy and reduce adverse effects.

P-13: Mass-producible sample sparing platform for microscopy shows that CD45RB ligation increases Treg

sensitivity to activation signals

Joanne H. Lee1, Jounghyun H. Lee1, and Lance C. Kam1

1Department of Biomedical Engineering, Columbia University, New York, NY, USA

Small subpopulations of cells, e.g. regulatory T cells, often play key roles in the function of the entire immune system.

While their smaller number makes them difficult to work with in conventional immunocytochemistry assays or flow

cytometry, microscopy can provide functional and spatial information on a single cell basis. Combined with surface

modification technology such as synthetic lipid bilayers and micropatterned antibodies, we are in a unique position

to be able to study the spatial mobility of intracellular signals (e.g. show that mobility of Lck differs between mouse

and human T cells). Even still, conventional microscopy platforms such as 96-well plates or flow cell systems

require a minimum of 10k to 1 million cells and does not allow for an interchangeable surface. Conical wells with a

1mm bottom and 5mm top diameter (microwells), laid out in a 96-well configuration were mass manufactured out

of polypropylene from Protolabs, and adhered to surface modified glass coverslips. 1k cells seeded and centrifuged

at 100g for 10 mins resulted in 81% of the cells landing on an image-able area. Based on the report that anti-CD45RB

mAb MB23G2 enhances graft-survival, we tested the hypothesis that anti-CD45RB ligation in vitro increases Treg

sensitivity to activation signals. 3 different activation signal levels (1, 5, and 20 µg/mL), 2 cell types, and 2 treatment

conditions conventionally required at least 150k cells per sample, or 1.8M cells total. On the microwell, we

performed the experiment with 8k cells per sample, with quadruplicates for a total of 384k cells, to show that the

ratio of phosphorylation of Lck at Tyr 394 to 505 sites, and alignment to micropatterned anti-CD3 dots are increased

in Tregs treated with anti-CD45RB.

P-14: Single cell pathway analysis to study resistant population after drug treatment, in ER+ breast cancer cells

with PIK3CA mutation

Sangkyun Lim, Caitlin E. Mills, Marc Hafner, Shu Wang, Peter K. Sorger

Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston,

MA 02115, USA

Email: [email protected]

One of the frustrating obstacles in cancer treatment is that cellular response to a given drug is heterogenous. While

many cells stop growing or die, there are cells that survive and continue to proliferate eventually. This fractional

response is observed in most of drug treatment, but the mechanism study specifically focusing on the resistant

population is challenging because the conventional assays are usually designed to monitor the whole population.

Here we performed cyclic immunofluorescence (cycIF) to monitor multiple cancer pathways at single cell level. By

co-staining with cell cycle markers, we could successfully distinguish the cycling cells from the non-cycling cells after

drug treatment and measure the activity of each pathway in six different subpopulations. By calculating the

Activation score for proliferation (AP), we identified the pathways that potentially control the proliferation in each

treatment. Some of the proteins identified were common in all four cell lines tested; for example, phospho-RB, Ki67,


and phospho-S6 were found to have high AP score in all the conditions, which is consistent with their key roles

during proliferation. On the other hand, we also observed some proteins were specific to particular cell lines or

conditions. Among them, ERK activity was found to be high in the cycling cells after co-treatment of ER antagonist

(Fulvestrant) and PI3Kinase inhibitor (Alpelisib/BYL719), only in BT483 and MCF7 cells. Further functional test

showed that MEK/ERK inhibitor (Trametinib) is effective only in BT483 and MCF7 cells and synergistic to Fulvestrant

and BYL719. Taken together, single cell pathway analysis with cycIF allowed to monitor major signaling pathways in

the specific populations in cell-cycle during drug response.

P-15: Targeting lytic and quiescent herpes simplex virus 1 genomes with CRISPR/Cas9

Hyung Suk Oh1, Magdalena Angelova1, Werner Neuhausser3, Kevin Eggan2, 3 and David M. Knipe1 1Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA, 2Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge,

Massachusetts, USA, 3Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge,

Massachusetts, USA

Email: [email protected]

Herpes simplex virus (HSV) 1 can undergo lytic replication or establish latency following primary infection. Although

there are several anti-HSV drugs that target lytic infection, no treatment is available to target latent HSV genomes

and prevent reactivation. Here we evaluated the use of the CRISPR (Clustered regularly-interspaced short

palindromic repeats)/Cas9 system to target HSV lytic and latent genomes. To study lytic infection, we established

human foreskin fibroblast (HFF) cell lines stably expressing Cas9 and guide RNAs (gRNAs) targeting essential HSV-1

genes, and infected the cells with HSV-1. Cas9/gRNA expression reduced viral yield by 2-4 logs compared to a control

cell line expressing Cas9 alone. We showed that Cas9/gRNA induced mutations in HSV genomes earlier than 6 hpi,

and the mutations accumulated over the viral replication. Interestingly, replicating HSV genomes are more prone to

editing than non-replicating HSV genomes. To test the ability of CRISPR/Cas9 system to target latent genomes, we

established a quiescent infection in HFFs with replication-defective HSV-1 d109. We transduced quiescently infected

cells with lentiviruses encoding Cas9/gRNA targeting essential viral genes, followed by reactivation with wildtype

HSV-1. We observed that reactivation of d109 from quiescent infection was reduced by 2-5 logs by single gRNAs or

combinations of gRNAs compared to the Cas9 control without gRNA. Additionally, we showed by deep sequencing

that quiescent HSV-1 genomes could be efficiently targeted and edited by Cas9/gRNA. This study demonstrates that

the CRISPR/Cas9 system can efficiently target lytic and latent HSV genomes.

P-16: Polarized transport through the Golgi complex for tumor invasiveness

Seung-Yeol Park

Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, and Department of Medicine,

Harvard Medical School, Boston, MA 02115 USA

Polarized transport of proteins and membrane to the cell surface promotes the tumor progression. The Golgi

complex plays a central role in intracellular transport. Previously, we elucidated that the polarized transport within

the Golgi complex is regulated by Cdc42 which had been known to control cell polarity. Notably, this ability of

Cdc42 helps to explain how it promotes cellular transformation. To understand further how the Golgi complex

contributes to tumor progression, we investigated signaling through the Ror2 receptor tyrosine kinase which

promotes invadopodia formation for tumor invasion. Here, we identified that intraflagellar transport 20 (IFT20)

regulates the nucleation of Golgi complex by affecting the GM130-AKAP450 complex, which promotes Golgi ribbon

formation in achieving polarized secretion for cell migration and invasion. Furthermore, IFT20 promotes the

efficiency of transport through the Golgi complex. These findings shed new insights into how Ror2 signaling


promotes tumor invasiveness, and also advance the understanding of how Golgi structure and transport can be

regulated.

P-17: Clonal heterogeneity within the myeloid lineage

Catherine Rhee and David Scadden

Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA; Center for Regenerative

Medicine and Cancer Center, Massachusetts General Hospital, MA

Email: [email protected]; Phone: 512-520-7272

Our tissues are not composed of morphologically and functionally homogenous cells. Rather, they are more

accurately described as complex mosaics. The hematopoietic system demonstrates heterogeneity, a cardinal feature

of healthy blood lost in diseased state. The condition of “clonal hematopoiesis of indeterminate potential (CHIP)” is

a risk factor of MDS and AML, and notably a risk for all-cause mortality and cardiovascular disease. This is postulated

to result in abnormal myeloid cells as progeny of diseased progenitors.

Our laboratory has developed a system for inducible clonal expansion of primary granulocyte-monocyte progenitors

(GMP) that can then proceed to full myeloid differentiation. Using this system to clonally expand progenitors enables

the study of myeloid cell heterogeneity. We have now found that each GMP clonal descendant behaves distinctively

to 6 unique challenges and cluster broadly into functional groups, each with distinct molecular characteristics. This

model permits the testing of clone-specific behaviors including sensitivity to leukemogenic alleles. We propose to

test whether the addition of the abnormal Tet2 and Asxl1 alleles associated with CHIP affect the in vitro and in vivo

behaviors of the clones, and validate which features correlate with pathogenic behaviors. This may reveal why some

clonal populations are non-pathogenic while others progress to disease, ultimately defining pro-pathogenic features

and blood stem cell therapeutic targets.

P-18: PLGA-bevacizumab implants for long-acting anti-VEGF efficacy in rabbit retinal vascular leakage model

Rae Sung Chang1, David A. Antonetti2, Jeffrey Jamison3, and Steven P. Schwendeman1

1 Department of Pharmaceutical Sciences and the Biointerfaces Institute, University of Michigan, Ann Arbor, MI

48109, 2Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI 48105, USA, 3Ophthy-DS, Inc., Kalamazoo, MI 49009, USA

E-mail: [email protected]; Phone: 734-730-1421

Wet age-related macular degeneration (AMD) is a major cause of vision loss among the elderly. In wet AMD, new

abnormal blood vessels grow under the macula, thus displacing the macula from its normal position, and resulting

in rapid central vision loss. Overexpression of vascular endothelial growth factor (VEGF) results in the growth of

abnormal blood vessels under the retina, and therefore, anti-VEGF therapy has become a potent treatment option

for wet AMD. Administration of the anti-VEGF agents is accomplished by intravitreal injections typically every 4

weeks, but this dosing frequency is problematic for patient convenience and compliance, and repeated intravitreal

injections may induce infection, inflammation and hemorrhage. Sustained release formulations of the anti-VEGF

agents can potentially reduce administration frequency for patient convenience and compliance, and minimize the

risks while maintaining the therapeutic concentration in the vitreous. Therefore, we developed injectable

poly(lactic-co-lycolic acid) (PLGA) implants which sustain the release of stable bevacizumab (Avastin®, anti-VEGF

monoclonal antibody (mAb)). An antacid (MgCO3) and trehalose were added to stabilize the encapsulated mAbs.

However, the presence of water-soluble trehalose in the implants creates high osmotic pressure, thus resulting in

fast release of mAbs. To sustain the release, therefore, pure PLGA was coated onto the lateral side of core implants.

The optimized implant formulations achieved high mAb loading (7.6 to 8.2 % w/w) and demonstrated continuous in

vitro release kinetics over six weeks with total cumulative release of 82 ± 8 to 89 ± 4 %. Little changes in monomer


content, immunoreactivity, and secondary structure of the released mAbs during the 6-week in vitro release period

were observed by size-exclusion high performance liquid chromatography, enzyme-linked immunosorbent assay,

and circular dichroism spectroscopy, respectively. Anti-VEGF efficacy of the optimized mAb implant was compared

to the same dose of free mAb in the rabbit VEGF-induced retinal leakage model (400 µg dose). Six weeks after

intravitreal injection of both formulations, only the mAb implant protected retinal blood vessels while significant

leakage was observed in the no-treatment control and free mAb groups. The retinal blood vessels of the implant

group were still protective over 8 weeks. Hence, this approach may be useful for development of long-acting anti-

VEGF therapy.


2018 KASBP SPRING JOB FAIR

The KASBP Spring Symposium offers a Job-Fair of full-service interviewing facility (private) for employers and career-

seekers. Currently, 7 companies participate in this Spring Symposium:

• Hanmi Pharm. Co., Ltd

• Green Cross & Mokam Life Science Research Center

• CKD

• Daegu Gyeongbuk Medical Innovation Foundation

• Qurient

How to Participate in the Career Service as an Applicant

The job-fair application was closed on May 25th. For a late-break application, please contact the KASBP Job-Fair

coordinator ([email protected]) to check the availability. Please bring your CV and documents that are

required by the company that you want to apply. The Job-Post of the companies is available from KASBP website

(under Announcement/Discussion).

Interview time is pre-arranged between 2:00 PM thru 5:00 PM on June 1st (Fri). If the time is not available, please

contact KASBP Job-Fair coordinator to arrange some other time. The interview locations will be notified separately

to the applicants via email.

2018 KASBP Spring-Symposium Registration is required. No additional fees are required to participate in Job-Fair as

an applicant.

2018 KASBP SPRING YOUNG GENERATION MENTORING PROGRAM

You are cordially invited to the 2nd Young Generation Mentoring Program at 2018 KASBP Spring Symposium, an

effort by KASBP to enhance the experience of Young Generation (YG) Members at KASBP Symposium. The

program allows YG Members to be connected with the mentor that matches with a specific field of study or areas

of concern.

Based on our 1st mentor/mentee program, we will have mentor-mentee meeting during 2018 KASBP Spring

Symposium.

2018 KASBP Spring Symposium Young Generation Committee.


PAST FELLOWSHIP AWARDEES

KASBP-DAEWOONG ACHIEVEMENT

2009 Jong Eun KIM (Gilead Sciences, Inc.), (Kainos Medicine Inc, Korea, Current)

2010 David C. CHU, (University of Georgia)

2011 Sung Ho KIM (University of California, Berkeley)

2012 Dennis Choi (Stony Brook Medicine and Stony Brook University)

2013 Joseph Kim (Inovio Pharmaceuticals)

2014 Kinam Park (Purdue University)

2015 Jong Sung Koh (Genoscco)

2016 Jang-Ho CHA (Novartis)

2017 Peter Park (Bicycle Therapeutics)

KASBP RECOGNITION AWARD

2015 Jong Wook Lee, Daewoong

KASBP-DAEWOONG FELLOWSHIP

2006 JaeKi MIN (New York University), Hahn KIM (Princeton University), HyeJin PARK (Rutgers University)

2007 JiSook MOON (Harvard University),SungYeon PARK (Rutgers University), SeokGeun LEE (Columbia University)

2008 HeungKyu LEE (Yale University), JungHwan KIM (Rutgers University), MinSik KANG (Columbia University)

2009 JinAh PARK (Harvard University), JaeMin CHOI (Yale University), DeokHo KIM (Johns Hopkins University)

2010 JungMin KEE (Rockefeller University), HyungWook KIM (NIH), SeJin AHN (Harvard University)

2011 MooRi HAN (University of California, LA), HwanJong JANG (Boston College)

2012 JeongHo JANG (Columbia University), JaeWoo CHOI (Oregon State University)

2013 JangEun Lee (University of Pennsylvania), Eun Chan Park (Rutgers University)

2014 Kimberly H. Kim (Harvard University), Seung Koo Lee (Weill Cornell Medical College), Min-Sik Kim (Johns

Hopkins University)

2015 Jiyeon Kim; UT Southwestern; Sun Mi Park, Memorial Sloan-Kettering Center); Byeong Seon Kim, University

of Pennsylvania

2016 Sang Bae Lee (Columbia University), Junil Kim (University of Pennsylvania), Ho-Keun Kwon (Harvard Medical

School)

2017 KyeongJin Kim, Ph.D. (Columbia University Medical Center), Min-Ji Bak, Ph.D. (Ernest Mario School of

Pharmacy), Heung Sik Hahm (Free University Berlin)

KASBP-GREEN CROSS FELLOWSHIP

2011 HanSang CHO (Harvard Medical School), SungWoong KANG (Johns Hopkins University), MiYeon KIM

(Columbia University), JaeYoung SOH (Rutgers University), SungYong HWANG (NIEHS/NIH)

2012 WonJin CHO (Drexel University), HyoJung KANG (Yale University), JungHyun LEE (Columbia University),

YongJae LEE (Yale University), JaeHyun YOON (NIH)

2013 Yunjong Lee (Johns Hopkins University), Jun-Dae Kim (Yale University)

Bae-Hoon Kim (Yale University) Ja Young Kim-Muller (Columbia University)

2014 Catherine Rhee (University of Texas at Austin), Ji-Seon Seo (The Rockefeller University) Sehyun Kim (New

York University)

2015 Young-Su Yi (New York University), Hee-Woong Lim (University of Pennsylvania), Bloria Bora Kim (The

Pennsylvania State University)

2016 Eui Tae Kim (University of Pennsylvania), Kihyun Lee (Weill Cornell Medical Science)


2017 Seung-Yeol Park, Ph.D. (Harvard medical school), Young Bok Abraham Kang, Ph.D. (Harvard medical school)

KASBP-HANMI FELLOWSHIP

2011 HyungJin AHN (Rockefeller University), ChangHoon CHO (Abramson Research Center)

2012 YuNa KIM (University of North Carolina), HyunSeob TAE (Yale University), InHye LEE (NIH)

2013 JooHee LEE (Memorial Sloan-Kettering Cancer Center), KyungRyun LEE (Rutgers University),

ManRyul LEE (Indiana University)

2014 Young Chan Cha (Wistar Institute), Min-Kyu Cho (New York University), Lark Kyun Kim, (Yale University),

Yu Shin Kim (Johns Hopkins University)

2015 Seonil Kim (New York University), Peter B. Kim (Yale University)

2016 Sungwhan Oh (Harvard Medical School), Won-Gil Lee (Yale University),

Hee-Jin Jeong (Harvard Medical School)

2017 Min-Kyung Choo (Harvard Medical School), Soo Seok Hwang (Yale University),

Heeoon Han (University of Pennsylvania)

KASBP-LG CHEM FELLOWSHIP

2017 Kyoung-Dong Kim, Ph.D. (Wistar Institute), Seok-Man Ho (Icahn School of Medicine at Mount Sinai)

KASBP-YUHAN FELLOWSHIP

2011 KiYoung KIM (Boston University), JoongSeop SHIM (Johns Hopkins University)

2012 YeMin HUH (University of Michigan), SookHee BANG (University of Pennsylvania), JungHo BAIK (Columbia

University)

2013 Dong Jun Lee (University of Chicago), Ingyu Kim (Yale University), Ja Yil Lee (Columbia University)

2014 Seouk Joon Kwon (Rensselaer Polytech Institute), Jeongmin Song (Yale University), Jae-Hyun Yang (Harvard

Medical School), Wan Seok Yang (Columbia University)

2015 Min-Joon Han (Harvard Medical School), Minjung Kang (Cornell University)

2016 Ki Su Kim (Harvard Medical School), Hongjae Sunwoo (Harvard Medical School), Seo-Young Park (University

of Massachusetts)

2017 Hanseul Yang (Rockefeller University), Ji-Hoon Park (NIH), Hong-Yeoul Ryu (Yale University)

KASBP-ST PHARM FELLOWSHIP

2016 Jung-Eun Jang (New York University), Byungsu Kwon (MIT)

KASBP FELLOWSHIP

2009 SangHo CHOI (NIH)

2010 SangRyung KIM (Columbia University), TaeSook YOON (Rutgers University), EunMi HUH (Cal. Tech.)

2015 Mi Jung Kim (Duke University), Minyoung Park (The Rockefeller University)

KASBP-KSEA FELLOWSHIP

2013 Sung In Lim (University of Virginia)

2014 Keun-woo Jin (Temple University)

KASBP-KUSCO FELLOWSHIP

2008 HyunHo KIM (National Institutes of Health), TaekBeom OHN (Harvard Medical School), WonAh JOO (Wistar

Institute)


KASBP-KRICT FELLOWSHIP

2009 SeungSik SHIN (Rutgers University), EunJoo JEONG (Columbia University), KyuWon BAEK (University of

Pennsylvania)

KASBP-KHIDI FELLOWSHIP

2010 JaeHyun BAE (Yale University), HeeYeon CHO (Boston College)

KASBP-DAEWOONG SCHOLARSHIP

2006 Jin K. PAI, Schering-Plough (Handok Pharmaceuticals, Korea, Current)

2007 YoungWhan PARK, Merck (National Cancer Center, Korea, Current)

2008 Young-Choon MOON (PTC Therapeutics)

2009 HongYong KIM (Novartis)

34 |P a g e 2 0 1 8 K A S B P F a l l S y m p o s i u m Preliminary Program

For more information, please visit www.kasbp.org

2018 KASBP Spring Symposium Attendees

Last

name

First name 한글이름 Affiliation Networking Group

1. Ahn Hae-Young 안해영 Ahn Bio Consulting PK/PD/pre-clinical/Clinical Science:

2. Aoyagi Kazuko Celerion PK/PD/pre-clinical/Clinical Science:

3. Bae Shingyu 배신규 MDimune Cell and Gene Therapy/Viral infection/Rare disease

4. Baek Kyuwon 백규원 AMO Lifescience Cell and Gene Therapy/Viral infection/Rare disease

5. Baek Yoonji 백윤지 MCPHS University PK/PD/pre-clinical/Clinical Science:

6. Chang Dong-Eun 장동은 CJ Research Center BD/Legal/VC:

7. Chang Hemmie 장혜미 Foley Hoag LLP

8. CHANG JIHOON 장지훈 Amgen Immuno-oncology/Autoimmune/Inflammatory

9. Chang Kern 장건희 Janssen Pharmaceutical Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

10. Chang Rae Sung 장래성 University of Michigan PK/PD/pre-clinical/Clinical Science:

11. CHO BRYAN KOTRA BD/Legal/VC: 12. CHO ILTAEG 조일택 Brigham and Women's Hospital Cell and Gene Therapy/Viral infection/Rare disease

13. Cho Jungmin 조정민 Curiosis Inc.

14. Cho Min-Kyu 조민규 Novartis Chemistry

15. Choe Mihee Lucia Roosevelt University Pharmacy 16. Choe Yun H. 최윤 Lucas and Mercanti, LLP BD/Legal/VC:

17. Choi Ashley 최효영 BWH Pharmacy

18. Choi Jun Young 최준영 Nitto Avecia

19. Choi Sun 최선아 University of Illinois at Chicago College of Pharmacy

Pharmacy

20. Choi Sung Hugh 최성휴 Genosco Cell and Gene Therapy/Viral infection/Rare disease

21. Choi Younggi 최영기 Alkermes BD/Legal/VC:

22. Choo Min-Kyung 추민경 MGH Immuno-oncology/Autoimmune/Inflammatory

23. Chung HaeWon 정해원 Sanofi Immuno-oncology/Autoimmune/Inflammatory

24. Chung Seungwon 정승원 AbbVie Chemistry

25. Cui Lian 최련 University of Pennsylvania Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

26. Dayma Yogesh 요게쉬 Koch institute, MIT Immuno-oncology/Autoimmune/Inflammatory

27. HAHM Sean 함성원 The Yakup Shinmoon BD/Legal/VC:

28. Han Sangyeul 한상열 Cell Signaling Technology PK/PD/pre-clinical/Clinical Science:

29. Han Sunny 한원선 Amyloid Solution Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

30. Hong Peter 홍성원 Regeneron Pharmaceuticals Immuno-oncology/Autoimmune/Inflammatory

31. Huh Eun Chul 허은철 GC Pharma BD/Legal/VC:

32. Huh Meena 허민아 Northeastern University Pharmacy

33. Hwang Amy 황유경 UIC college of pharmacy Pharmacy

34. Hwang Jae Yeon 황재연 Yale University, School of Medicine

35. Hwang Ji Young 황지영 Geisel School of Medicine at Dartmouth

Immuno-oncology/Autoimmune/Inflammatory

36. Hwang So-Young 황소영 Genosco Immuno-oncology/Autoimmune/Inflammatory

37. HYUN LEE 이현 SM-Sino Technology Investment PK/PD/pre-clinical/Clinical Science:

38. Ihm Juliana 임해연 UIC college of Pharmacy Pharmacy

39. Jeon Ok Hee 전옥희 연세의료원


Last

name


40. Jeong Euy-Myoung Brown University Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

41. Jeong Jae Uk 정재욱 GSK Chemistry

42. Jeong Vincent 정영관 Yuanta Investment BD/Legal/VC:

43. Jo Seunghee 조승희 Agios Pharmaceuticals Cell and Gene Therapy/Viral infection/Rare disease

44. Jung Dan 정후영 VISIONMED USA BD/Legal/VC:

45. Jung Jihae 정지혜 Northeastern University Pharmacy

46. Jung Young Chun 정영춘 Akebia Therapeutics Inc. Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

47. Kang Byoung Cheol 강병철 DONGWHA PHARM. BD/Legal/VC:

48. Kang Byungseok 강병석 KBioHealth

49. Kang Soeun 강소은 University of Illinois at Chicago Pharmacy

50. Kang Tony 강성우 Navitor Pharmaceuticals

51. KIM AMI 김아미 동화약품 BD/Legal/VC:

52. Kim Bokyung 김보경 University of IL at Chicago-College of Pharmacy

Pharmacy

53. KIM BUMJUN 김범준 Northeastern University Pharmacy

54. Kim Dae-Shik 김대식 Eisai Inc Chemistry

55. Kim Do Hyung 김도형 Johns Hopkins University Immuno-oncology/Autoimmune/Inflammatory

56. Kim Fred 김병철 VISIONMED, LTD BD/Legal/VC:

57. Kim Gyuri 김규리 Northeastern University Pharmacy

58. KIM HOONJOO 김훈주 DGMIF Pharmacy

59. KIM HYUNKI 김현기 Stonebridge Ventures BD/Legal/VC:

60. Kim Jaeah University of Georgia PK/PD/pre-clinical/Clinical Science: 61. Kim Jae-Hun 김재훈 IFF Chemistry

62. Kim Jeongseok 김정석 Boston University

63. Kim Jisu 김지수 Massachusetts college of pharmacy Pharmacy

64. Kim Jiwoo 김지우 Northeastern University PK/PD/pre-clinical/Clinical Science:

65. Kim John 김종민 Nova Biomedical BD/Legal/VC:

66. Kim Joo Yeon 김주연 MIT Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

67. Kim Joonyul 김준열 Proximity Biosciences LLC BD/Legal/VC:

68. Kim Juny 김주은 CRScube America BD/Legal/VC:

69. Kim Ki Don 김기돈 CRScube BD/Legal/VC:

70. Kim Kiel 김기일 NS Investment BD/Legal/VC:

71. Kim Sahee 김사희 RevHealth Pharmacy

72. Kim Sangdoo 김상두 Harvard Medical School Immuno-oncology/Autoimmune/Inflammatory

73. Kim Sean 김승빈 Blueprint Medicines PK/PD/pre-clinical/Clinical Science:

74. KIM SEWON 김세원 GENOSCO

75. Kim Sung ki 김성기 MCPHS university Pharmacy

76. KIM SUNGIL 김성일 아모라이프사이언스 Immuno-oncology/Autoimmune/Inflammatory

77. Kim Sung-Kwon 김성권 Alexion Pharmaceuticals Immuno-oncology/Autoimmune/Inflammatory

78. Kim Taeg 김택 Bristol-Myers Squibb

79. Kim Younghoon 김영훈 Sanofi-Genzyme Cell and Gene Therapy/Viral infection/Rare disease

80. kim youngjin 김영진 rockefeller university Immuno-oncology/Autoimmune/Inflammatory

81. Kim Youngsun 김영선 Adello Biologics PK/PD/pre-clinical/Clinical Science:


Last

name


82. Kong Philip 공필립 Yale University BD/Legal/VC:

83. KWEON DON SUN 권돈선 Woori Technology Inc PK/PD/pre-clinical/Clinical Science:

84. KWON HOKEUN 권호근 Harvard Medical School Immuno-oncology/Autoimmune/Inflammatory

85. Kwon Paul Novartis 86. Laramy Janice 이경미 Novartis PK/PD/pre-clinical/Clinical Science:

87. Lee Byoung-Chul 이병철 23andMe, Inc. PK/PD/pre-clinical/Clinical Science:

88. LEE BYUNG-CHUL 이병철 GENECAST Immuno-oncology/Autoimmune/Inflammatory

89. Lee Dooyoung 이두영 Applied BioMath PK/PD/pre-clinical/Clinical Science:

90. Lee Eon Soo 이언수 New Jersey Institute of Technology BD/Legal/VC:

91. Lee Heedoo 이희두 Pulmonary Center, Boston University School of Medicine, Boston

Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

92. Lee Hyun-Hee 이현희 Merck Immuno-oncology/Autoimmune/Inflammatory

93. LEE JAEKYOO 이재규 GENOSCO Immuno-oncology/Autoimmune/Inflammatory

94. LEE JAEWON 이재원 CHONG KUN DANG PHARM. Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

95. Lee James 이석호 Ironwood Pharmaceuticals Inc. BD/Legal/VC:

96. Lee Ji Yoon 이지윤 Northeastern University Pharmacy

97. Lee JiEun 이지은 Mcphs PK/PD/pre-clinical/Clinical Science:

98. Lee Jisoo 이지수 대학원생 Pharmacy

99. Lee Jungeun 이정은 Northeastern University Pharmacy

100. Lee Kwangho 이광호 KRICT (한국화학연구원) Immuno-oncology/Autoimmune/Inflammatory

101. Lee Kyuhong 이규홍 Korea Institute of Toxicology Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

102. Lee Lauren Young-Mi

이영미 한미약품 BD/Legal/VC:

103. Lee Michael 이명렬 Amolifescience co. ltd Cell and Gene Therapy/Viral infection/Rare disease

104. Lee Sang Hoon 이상훈 ABL Bio Immuno-oncology/Autoimmune/Inflammatory

105. Lee Seungkyu 이승규 Boston Children's Hospital Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

106. Lee Song Ee 이송이 MDimune Cell and Gene Therapy/Viral infection/Rare disease

107. Lee Sunhee 이선희 Albert Einstein college of medicine Immuno-oncology/Autoimmune/Inflammatory

108. Lee Sun-Hwa 이선화 대구경북첨단의료산업진흥재단

(DGMIF)

Cell and Gene Therapy/Viral infection/Rare disease

109. Lee Yong Seok 이용석 Center for Advancing Cancer Therapeutics, Asan Medical Center

PK/PD/pre-clinical/Clinical Science:

110. Lim Hanjo 임한조 Genentech PK/PD/pre-clinical/Clinical Science:

111. Lim Hyungwook 임형욱 Novartis Institutes for Biomedical Research


112. Lim Jaeseung 임재승 Cellatoz Therapeutics, Inc. Cell and Gene Therapy/Viral infection/Rare disease

113. Lim Sang Kyun 임상균 Harvard Medical School PK/PD/pre-clinical/Clinical Science:

114. Lim Sungtaek 임성택 Sanofi Pharmaceuticals Chemistry

115. Ma Sunghoon 마성훈 Exelixis Chemistry

116. Moon Young-choon 문영춘 PTC Therapeutics Cell and Gene Therapy/Viral infection/Rare disease

117. Nam Kiyean 남기연 Qurient Co. Ltd. Immuno-oncology/Autoimmune/Inflammatory

118. Oh Chris Chigon 오치곤 ENVIGO BD/Legal/VC:

119. Oh Hyungsuk 오형석 Harvard medical School Cell and Gene Therapy/Viral infection/Rare disease

120. Paik Ik-Hyeon 백익현 WAVE Life Sciences, Inc. Chemistry

121. Park Chanwoo 박찬우 Northeastern University Pharmacy


Last

name


122. Park Gusun 박구선 오송첨단의료산업진흥재단

123. Park Jennifer Sang-ha Applied BioMath PK/PD/pre-clinical/Clinical Science: 124. Park JiYoung 박지영 Rutgers University BD/Legal/VC:

125. Park Kihyo 박기효 GC Pharma (녹십자) BD/Legal/VC:

126. Park Peter 박정수 Harvard Medical School

127. Park Saejeong 박세정 YCRC PK/PD/pre-clinical/Clinical Science:

128. Park Sang Tae 박상태 Macrogen Clinical Laboratory BD/Legal/VC:

129. PARK SEIL 박세일 YONSEI UNIVERSITY COLLEGE OF MEDICINE

PK/PD/pre-clinical/Clinical Science:

130. Park Seung-Yeol 박승열 BWH Cell and Gene Therapy/Viral infection/Rare disease

131. Park Sohyun 박소현 northeastern university Pharmacy

132. Park Sunmin 박선민 CVS Pharmacy Pharmacy

133. Park Young-Seoub 박영섭 Green Cross BD/Legal/VC:

134. Rhee So Hyun 이소현 Celgene Immuno-oncology/Autoimmune/Inflammatory

135. Rho Gab Seon 노갑선 Woori Technology Inc PK/PD/pre-clinical/Clinical Science:

136. Rim Nicholas 임내균 Novartis Immuno-oncology/Autoimmune/Inflammatory

137. Ryu Joonsoo 류준수 GC 녹십자 BD/Legal/VC:

138. Ryu Keun Ho 유근호 종근당 PK/PD/pre-clinical/Clinical Science:

139. SEEN Dongseung 신동승 GPCR Therapeutics, Inc. Immuno-oncology/Autoimmune/Inflammatory

140. Seo Jiwon 서지원 Northeastern University Pharmacy School

Pharmacy

141. SHEEN JOON HO 신준호 LG Chem Life Sciences Immuno-oncology/Autoimmune/Inflammatory

142. Shim Jaehoon 심재훈 Boston Children's Hospital PK/PD/pre-clinical/Clinical Science:

143. Shin Baehyun 신배현 Massachusetts General Hospital Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

144. SHIN HYEON JUN 신현준 Yale University

145. Shin Hyunjin (Gene)

신현진 Takeda Pharmaceuticals International Co.


146. Shin Soo 신숙일 DWK lifesciences Chemistry

147. SIM BOKYUNG 심보경 Osong Medical Innovation Foundation

148. Sohn Jung-woo 손정우 ATCC Center for Translational Microbiology

149. Son Ikbae 손익배 Catalent Biologics Chemistry

150. Son Ji Min 손지민 Student Pharmacy

151. Son Min Young 손민영 NewYork-Presbyterian/Columbia University Medical Center

152. SON MOON-HO 손문호 대구경북첨단의료산업진흥재단 신약개발지원센터(DGMIF)

Cell and Gene Therapy/Viral infection/Rare disease

153. Song Andy Byungho 송병호 Cellatoz Therapeutics, Inc. Cell and Gene Therapy/Viral infection/Rare disease

154. Song HoJuhn 송호준 Genosco BD/Legal/VC:

155. Song Mina 송민아 N/A Pharmacy

156. Song Saeheum 송세흠 DaiichiSankyo

157. Suh Byung-Chul (Ben)

서병철 Enanta Pharmaceuticals, Inc Chemistry

158. Suh Hyunsuk 서현석 Pfizer PK/PD/pre-clinical/Clinical Science:

159. Suh K. Stephen 서광순 Hackensack Meridian Health BD/Legal/VC:

160. Sung Moo Je 성무제 Novartis Chemistry


Last

name


161. Um Moonkyoung 엄문경 Mintz Levin BD/Legal/VC:

162. Won Doyon 원도연 Nutter McClennen & Fish Immuno-oncology/Autoimmune/Inflammatory

163. Yang Stephanie 양현영 Northeastern University Pharmacy

164. yim yeong shin 임영신 MIT Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

165. Yoo Bora 유보라 The Forsyth Institute Immuno-oncology/Autoimmune/Inflammatory

166. Yoo Hyouna 윤현아 GC Pharma Cell and Gene Therapy/Viral infection/Rare disease

167. Yoo Lang 유랑 Nathan Kline Institute/NYU College of Medicine

Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

168. Yoon Young-Mee 윤영미 Asan Medical Center, T2B (Center for Advancing Cancer Therapeutics, CACT)


169. You Dahea (Diana) 유다혜 Rutgers University PK/PD/pre-clinical/Clinical Science:

170. You Kwontae 유권태 Broad Institute Immuno-oncology/Autoimmune/Inflammatory

171. Yu Chung Jong Harvard Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

172. Yu Mikyung 유미경 BWH/HMS Immuno-oncology/Autoimmune/Inflammatory

173. Yun Hoyoung 윤호영 Curiosis, Inc.

174. Yun Kangsik 윤강식 국가항암신약개발사업단 BD/Legal/VC:

Networking Group Last

name

First name 한글이름 Affiliation

9 Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Chang Kern 장건희 Janssen Pharmaceutical


Cui Lian 최련 University of Pennsylvania


Han Sunny 한원선 Amyloid Solution


Jeong Euy-Myoung Brown University


Jung Young Chun 정영춘 Akebia Therapeutics Inc.


Kim Joo Yeon 김주연 MIT


Lee Heedoo 이희두 Pulmonary Center, Boston University School of Medicine, Boston


LEE JAEWON 이재원 CHONG KUN DANG PHARM.


Lee Kyuhong 이규홍 Korea Institute of Toxicology


Lee Seungkyu 이승규 Boston Children's Hospital


Shin Baehyun 신배현 Massachusetts General Hospital


yim yeong shin 임영신 MIT


Yoo Lang 유랑 Nathan Kline Institute/NYU College of Medicine


Yu Chung Jong Harvard

1 PK/PD/pre-clinical/Clinical Science: Ahn Hae-Young 안해영 Ahn Bio Consulting

2 PK/PD/pre-clinical/Clinical Science: Aoyagi Kazuko Celerion 5 PK/PD/pre-clinical/Clinical Science: Baek Yoonji 백윤지 MCPHS University

10 PK/PD/pre-clinical/Clinical Science: Chang Rae Sung 장래성 University of Michigan

28 PK/PD/pre-clinical/Clinical Science: Han Sangyeul 한상열 Cell Signaling Technology



name


37 PK/PD/pre-clinical/Clinical Science: HYUN LEE 이현 SM-Sino Technology Investment

60 PK/PD/pre-clinical/Clinical Science: Kim Jaeah University of Georgia 64 PK/PD/pre-clinical/Clinical Science: Kim Jiwoo 김지우 Northeastern University

73 PK/PD/pre-clinical/Clinical Science: Kim Sean 김승빈 Blueprint Medicines

81 PK/PD/pre-clinical/Clinical Science: Kim Youngsun 김영선 Adello Biologics

83 PK/PD/pre-clinical/Clinical Science: KWEON DON SUN 권돈선 Woori Technology Inc

86 PK/PD/pre-clinical/Clinical Science: Laramy Janice 이경미 Novartis

87 PK/PD/pre-clinical/Clinical Science: Lee Byoung-Chul 이병철 23andMe, Inc.

89 PK/PD/pre-clinical/Clinical Science: Lee Dooyoung 이두영 Applied BioMath

97 PK/PD/pre-clinical/Clinical Science: Lee JiEun 이지은 Mcphs

109 PK/PD/pre-clinical/Clinical Science: Lee Yong Seok 이용석 Center for Advancing Cancer Therapeutics, Asan Medical Center

110 PK/PD/pre-clinical/Clinical Science: Lim Hanjo 임한조 Genentech

113 PK/PD/pre-clinical/Clinical Science: Lim Sang Kyun 임상균 Harvard Medical School

123 PK/PD/pre-clinical/Clinical Science: Park Jennifer Sang-ha Applied BioMath 127 PK/PD/pre-clinical/Clinical Science: Park Saejeong 박세정 YCRC

129 PK/PD/pre-clinical/Clinical Science: PARK SEIL 박세일 YONSEI UNIVERSITY COLLEGE OF MEDICINE

135 PK/PD/pre-clinical/Clinical Science: Rho Gab Seon 노갑선 Woori Technology Inc

138 PK/PD/pre-clinical/Clinical Science: Ryu Keun Ho 유근호 종근당

142 PK/PD/pre-clinical/Clinical Science: Shim Jaehoon 심재훈 Boston Children's Hospital

158 PK/PD/pre-clinical/Clinical Science: Suh Hyunsuk 서현석 Pfizer

169 PK/PD/pre-clinical/Clinical Science: You Dahea (Diana) 유다혜 Rutgers University

15 Pharmacy Choe Mihee Lucia Roosevelt University 17 Pharmacy Choi Ashley 최효영 BWH

19 Pharmacy Choi Sun 최선아 University of Illinois at Chicago College of Pharmacy

32 Pharmacy Huh Meena 허민아 Northeastern University

33 Pharmacy Hwang Amy 황유경 UIC college of pharmacy

38 Pharmacy Ihm Juliana 임해연 UIC college of Pharmacy

45 Pharmacy Jung Jihae 정지혜 Northeastern University

49 Pharmacy Kang Soeun 강소은 University of Illinois at Chicago

52 Pharmacy Kim Bokyung 김보경 University of IL at Chicago-College of Pharmacy

53 Pharmacy KIM BUMJUN 김범준 Northeastern University

57 Pharmacy Kim Gyuri 김규리 Northeastern University

58 Pharmacy KIM HOONJOO 김훈주 DGMIF

63 Pharmacy Kim Jisu 김지수 Massachusetts college of pharmacy

71 Pharmacy Kim Sahee 김사희 RevHealth

75 Pharmacy Kim Sung ki 김성기 MCPHS university

96 Pharmacy Lee Ji Yoon 이지윤 Northeastern University

98 Pharmacy Lee Jisoo 이지수 대학원생

99 Pharmacy Lee Jungeun 이정은 Northeastern University

121 Pharmacy Park Chanwoo 박찬우 Northeastern University

131 Pharmacy Park Sohyun 박소현 northeastern university

132 Pharmacy Park Sunmin 박선민 CVS Pharmacy

140 Pharmacy Seo Jiwon 서지원 Northeastern University Pharmacy School



name


150 Pharmacy Son Ji Min 손지민 Student

155 Pharmacy Song Mina 송민아 N/A

163 Pharmacy Yang Stephanie 양현영 Northeastern University

8 Immuno-oncology/Autoimmune/Inflammatory CHANG JIHOON 장지훈 Amgen

22 Immuno-oncology/Autoimmune/Inflammatory Choo Min-Kyung 추민경 MGH

23 Immuno-oncology/Autoimmune/Inflammatory Chung HaeWon 정해원 Sanofi

26 Immuno-oncology/Autoimmune/Inflammatory Dayma Yogesh 요게쉬 Koch institute, MIT

30 Immuno-oncology/Autoimmune/Inflammatory Hong Peter 홍성원 Regeneron Pharmaceuticals

35 Immuno-oncology/Autoimmune/Inflammatory Hwang Ji Young 황지영 Geisel School of Medicine at Dartmouth

36 Immuno-oncology/Autoimmune/Inflammatory Hwang So-Young 황소영 Genosco

55 Immuno-oncology/Autoimmune/Inflammatory Kim Do Hyung 김도형 Johns Hopkins University

72 Immuno-oncology/Autoimmune/Inflammatory Kim Sangdoo 김상두 Harvard Medical School

76 Immuno-oncology/Autoimmune/Inflammatory KIM SUNGIL 김성일 아모라이프사이언스

77 Immuno-oncology/Autoimmune/Inflammatory Kim Sung-Kwon 김성권 Alexion Pharmaceuticals

80 Immuno-oncology/Autoimmune/Inflammatory kim youngjin 김영진 rockefeller university

84 Immuno-oncology/Autoimmune/Inflammatory KWON HOKEUN 권호근 Harvard Medical School

88 Immuno-oncology/Autoimmune/Inflammatory LEE BYUNG-CHUL 이병철 GENECAST

92 Immuno-oncology/Autoimmune/Inflammatory Lee Hyun-Hee 이현희 Merck

93 Immuno-oncology/Autoimmune/Inflammatory LEE JAEKYOO 이재규 GENOSCO

100 Immuno-oncology/Autoimmune/Inflammatory Lee Kwangho 이광호 KRICT (한국화학연구원)

104 Immuno-oncology/Autoimmune/Inflammatory Lee Sang Hoon 이상훈 ABL Bio

107 Immuno-oncology/Autoimmune/Inflammatory Lee Sunhee 이선희 Albert Einstein college of medicine

111 Immuno-oncology/Autoimmune/Inflammatory Lim Hyungwook 임형욱 Novartis Institutes for Biomedical Research

117 Immuno-oncology/Autoimmune/Inflammatory Nam Kiyean 남기연 Qurient Co. Ltd.

134 Immuno-oncology/Autoimmune/Inflammatory Rhee So Hyun 이소현 Celgene

136 Immuno-oncology/Autoimmune/Inflammatory Rim Nicholas 임내균 Novartis

139 Immuno-oncology/Autoimmune/Inflammatory SEEN Dongseung 신동승 GPCR Therapeutics, Inc.

141 Immuno-oncology/Autoimmune/Inflammatory SHEEN JOON HO 신준호 LG Chem Life Sciences

145 Immuno-oncology/Autoimmune/Inflammatory Shin Hyunjin (Gene)

신현진 Takeda Pharmaceuticals International Co.

162 Immuno-oncology/Autoimmune/Inflammatory Won Doyon 원도연 Nutter McClennen & Fish

165 Immuno-oncology/Autoimmune/Inflammatory Yoo Bora 유보라 The Forsyth Institute

168 Immuno-oncology/Autoimmune/Inflammatory Yoon Young-Mee 윤영미 Asan Medical Center, T2B (Center for Advancing Cancer Therapeutics, CACT)

170 Immuno-oncology/Autoimmune/Inflammatory You Kwontae 유권태 Broad Institute

172 Immuno-oncology/Autoimmune/Inflammatory Yu Mikyung 유미경 BWH/HMS

14 Chemistry Cho Min-Kyu 조민규 Novartis

24 Chemistry Chung Seungwon 정승원 AbbVie

41 Chemistry Jeong Jae Uk 정재욱 GSK

54 Chemistry Kim Dae-Shik 김대식 Eisai Inc

61 Chemistry Kim Jae-Hun 김재훈 IFF

114 Chemistry Lim Sungtaek 임성택 Sanofi Pharmaceuticals

115 Chemistry Ma Sunghoon 마성훈 Exelixis

120 Chemistry Paik Ik-Hyeon 백익현 WAVE Life Sciences, Inc.



name


146 Chemistry Shin Soo 신숙일 DWK lifesciences

149 Chemistry Son Ikbae 손익배 Catalent Biologics

157 Chemistry Suh Byung-Chul (Ben)

서병철 Enanta Pharmaceuticals, Inc

160 Chemistry Sung Moo Je 성무제 Novartis

3 Cell and Gene Therapy/Viral infection/Rare disease Bae Shingyu 배신규 MDimune

4 Cell and Gene Therapy/Viral infection/Rare disease Baek Kyuwon 백규원 AMO Lifescience

12 Cell and Gene Therapy/Viral infection/Rare disease CHO ILTAEG 조일택 Brigham and Women's Hospital

20 Cell and Gene Therapy/Viral infection/Rare disease Choi Sung Hugh 최성휴 Genosco

43 Cell and Gene Therapy/Viral infection/Rare disease Jo Seunghee 조승희 Agios Pharmaceuticals

79 Cell and Gene Therapy/Viral infection/Rare disease Kim Younghoon 김영훈 Sanofi-Genzyme

103 Cell and Gene Therapy/Viral infection/Rare disease Lee Michael 이명렬 Amolifescience co. ltd

106 Cell and Gene Therapy/Viral infection/Rare disease Lee Song Ee 이송이 MDimune

108 Cell and Gene Therapy/Viral infection/Rare disease Lee Sun-Hwa 이선화 대구경북첨단의료산업진흥재단(DGMIF)

112 Cell and Gene Therapy/Viral infection/Rare disease Lim Jaeseung 임재승 Cellatoz Therapeutics, Inc.

116 Cell and Gene Therapy/Viral infection/Rare disease Moon Young-choon 문영춘 PTC Therapeutics

119 Cell and Gene Therapy/Viral infection/Rare disease Oh Hyungsuk 오형석 Harvard medical School

130 Cell and Gene Therapy/Viral infection/Rare disease Park Seung-Yeol 박승열 BWH

152 Cell and Gene Therapy/Viral infection/Rare disease SON MOON-HO 손문호 대구경북첨단의료산업진흥재단 신약개발지원센터 (DGMIF)

153 Cell and Gene Therapy/Viral infection/Rare disease Song Andy Byungho 송병호 Cellatoz Therapeutics, Inc.

166 Cell and Gene Therapy/Viral infection/Rare disease Yoo Hyouna 윤현아 GC Pharma

6 BD/Legal/VC: Chang Dong-Eun 장동은 CJ Research Center

11 BD/Legal/VC: CHO BRYAN KOTRA 16 BD/Legal/VC: Choe Yun H. 최윤 Lucas and Mercanti, LLP

21 BD/Legal/VC: Choi Younggi 최영기 Alkermes

27 BD/Legal/VC: HAHM Sean 함성원 The Yakup Shinmoon

31 BD/Legal/VC: Huh Eun Chul 허은철 GC Pharma

42 BD/Legal/VC: Jeong Vincent 정영관 Yuanta Investment

44 BD/Legal/VC: Jung Dan 정후영 VISIONMED USA

47 BD/Legal/VC: Kang Byoung Cheol 강병철 DONGWHA PHARM.

51 BD/Legal/VC: KIM AMI 김아미 동화약품

56 BD/Legal/VC: Kim Fred 김병철 VISIONMED, LTD

59 BD/Legal/VC: KIM HYUNKI 김현기 Stonebridge Ventures

65 BD/Legal/VC: Kim John 김종민 Nova Biomedical

67 BD/Legal/VC: Kim Joonyul 김준열 Proximity Biosciences LLC

68 BD/Legal/VC: Kim Juny 김주은 CRScube America

69 BD/Legal/VC: Kim Ki Don 김기돈 CRScube

70 BD/Legal/VC: Kim Kiel 김기일 NS Investment

82 BD/Legal/VC: Kong Philip 공필립 Yale University

90 BD/Legal/VC: Lee Eon Soo 이언수 New Jersey Institute of Technology

95 BD/Legal/VC: Lee James 이석호 Ironwood Pharmaceuticals Inc.

102 BD/Legal/VC: Lee Lauren Young-Mi

이영미 한미약품



name


118 BD/Legal/VC: Oh Chris Chigon 오치곤 ENVIGO

124 BD/Legal/VC: Park JiYoung 박지영 Rutgers University

125 BD/Legal/VC: Park Kihyo 박기효 GC Pharma (녹십자)

128 BD/Legal/VC: Park Sang Tae 박상태 Macrogen Clinical Laboratory

133 BD/Legal/VC: Park Young-Seoub 박영섭 Green Cross

137 BD/Legal/VC: Ryu Joonsoo 류준수 GC 녹십자

154 BD/Legal/VC: Song HoJuhn 송호준 Genosco

159 BD/Legal/VC: Suh K. Stephen 서광순 Hackensack Meridian Health

161 BD/Legal/VC: Um Moonkyoung 엄문경 Mintz Levin

174 BD/Legal/VC: Yun Kangsik 윤강식 국가항암신약개발사업단

7 Chang Hemmie 장혜미 Foley Hoag LLP

13 Cho Jungmin 조정민 Curiosis Inc.

18 Choi Jun Young 최준영 Nitto Avecia

34 Hwang Jae Yeon 황재연 Yale University, School of Medicine

39 Jeon Ok Hee 전옥희 연세의료원

48 Kang Byungseok 강병석 KBioHealth

50 Kang Tony 강성우 Navitor Pharmaceuticals

62 Kim Jeongseok 김정석 Boston University

74 KIM SEWON 김세원 GENOSCO

78 Kim Taeg 김택 Bristol-Myers Squibb

85 Kwon Paul Novartis 122 Park Gusun 박구선 오송첨단의료산업진흥재단

126 Park Peter 박정수 Harvard Medical School

144 SHIN HYEON JUN 신현준 Yale University

147 SIM BOKYUNG 심보경 Osong Medical Innovation Foundation

148 Sohn Jung-woo 손정우 ATCC Center for Translational Microbiology

151 Son Min Young 손민영 NewYork-Presbyterian/Columbia University Medical Center

156 Song Saeheum 송세흠 DaiichiSankyo

173 Yun Hoyoung 윤호영 Curiosis, Inc.

Documents

2018 KASBP Spring Symposium Program v3 Spring... · 2018. 6. 4. · SeanKim, Jae Uk Jeong Website and SNS Management Committee Daeho Lee Sahee Kim, Sohyun Aria Rhee, Jiyoung Jamie