T A R G E T I N G S E R I O U S D I S E A S E S O F I M M U N O - I N F L A M M A T I O N A N D F I B R O S I S

June 2016

NASDAQ: TBRA

Corporate Presentation

Forward Looking Statements

This presentation and other matters discussed today or answers that may be given in response to questions may include statements that are, or may be deemed, “forward-looking statements.” Any statements that we make today, other than historical facts, are forward looking statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, included in this presentation regarding our future results of operations and financial position, strategy and plans, and our expectations for future operations are forward-looking statements. In some cases, you can identify forward-looking statements by terms such as “believe,” “may,” “will,” “estimate,” “continue,” “anticipate,” “design,” “intend,” “expect,” “could,” “plan,” “potential,” “predict,” “seek,” “should,” “would” or the negative version of these words and similar expressions intended to identify forward-looking statements, and similar expression and comparable terminology intended to identify forward-looking statements.

Forward-looking statements reflect management's current expectations, are based on certain assumptions and involve certain risks and uncertainties. Forward-looking statements include, but are not limited to, statements about: financial projections and estimates and their underlying assumptions, including, without limitation, sufficiency of our cash resources and needs for and ability to obtain additional financing; anticipated timing of patient enrollment in our clinical studies and availability of clinical data; anticipated timing of completing our clinical studies; the size and growth of our potential patient population; the mechanism of action of our product candidates; the ability to obtain and maintain regulatory approval of our product candidates; and the timing and success of the development and commercialization of our anticipated product candidates and the availability of alternative therapies for our target market. The Company's actual results could differ materially from those anticipated in these forward-looking statements as a result of various factors. Additional information regarding factors that could cause results to differ are available in the Company's other periodic filings with the SEC.

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Changing the Course of NASH & Liver Disease

3

Building a leading NASH program• Cenicriviroc (CVC) Phase 2b CENTAUR data Q3 2016• Evogliptin (EVO) + CVC combination study planned for 2016

Building long-term value• Transition to Phase 3 for CVC single-agent, combinations to follow• Q1 2016 cash balance: $53 million; cash runway to H2 2017

CVC: potent immuno-inflammatory agent• Once-daily dosing & favorable safety profile; cornerstone potential for NASH• Phase 2 in Primary Sclerosing Cholangitis: potential to be disease modifying

Leading NASH Program, Growth Potential Across Immuno-inflammatory Diseases

4

NASH and Supporting Clinical StudiesCENTAUR Phase 2b Primary endpoint Q3 2016

ORION Phase 2a Metabolic parameters, full data Q4 2016

Phase 3 enabling studies Ongoing

NASH CombinationsCVC + EVO Clinical studies to start 2016

Other Combination Studies

Other Immuno-inflammationPERSEUS – Primary Sclerosing Cholangitis (PSC) Enrolling

Diabetic nephropathy Key markers for kidney function to be measured in NASH P2b

Oncology

HIVHIV (Anti-retroviral) Phase 2b completed

HIV (Immuno-inflammation) – Adjunctive Care Settings

PRECLINICAL PHASE 1 PHASE 2 PHASE 3

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NASH Unmet Need

Obesity is Rapidly Increasing Among US adults1

61. CDC. Behavioral Risk Factor Surveillance System (BMI ≥30, or about 30 lbs. overweight for 5’4” person); 2. Wong et al. 2015

No Data

<14%

14%–17.9%

18%–21.9%

22%–25.9%

≥26%

2013

1994

2000

NASH is now the second most common indication

for liver transplant2

NASH: A Severe Form of Fatty Liver Disease

CirrhosisHCC

Liver FailureDeath

High-riskNASH

NAFLD + inflammation and fibrosis type 2 diabetes,

high BMI

6 –10m affected5

At greatest risk of progression to cirrhosis

or other serious liver conditions

NAFLDHealthy NASHNAFLD + inflammation

1. Matteoni et al. 1999; 2. Wree et al. 2013; 3. Vernon et al. 2011; 4. Schattenberg et al. 2011; 5. Angulo et al. 1999

86 – 108min USA2,3

9 –15min USA4

Focus of CVC clinical developmentPhase 2b CENTAUR Study

7

8

CVC for NASH

Profile of An Ideal Product for NASH

9

Target cause of damage & fibrosis

Anti-fibrotic & anti-inflammatory

Safe for chronic setting

Oral, combinable

CCR2 & CCR5 central in inflammatory and fibrotic pathways and insulin resistance

Improvement in sCD14, ELF, APRI & FIB-4

Reduced fibrosis across multiple models

600+ subjects treated to date, 115 up to 48 weeks

Well tolerated; Few drug-related AEs

30-40 hour half life

One pill, once-daily formulation

Ideal Attribute CVC Evidence

FibrosisInflammation

The Molecular Engines that drive NASH

Adapted from Arun Sanyal, NASH Symposium Paris June 2015

NAFLDNASH

Cirrhosis HCCMetabolic

Abnormality

10

CVC Targets Inflammation & Fibrogenesis

11 Friedman, S. et al., Contemporary Clinical Trials, 47, March 2016

Metabolic-driven liver injury

Evokes inflammatory

response

And fibrogenesis

CVC Mechanism

Block overactive inflammatory

signaling

Disrupt signaling to activate stellate

cells

Hepatic Stellate Cell activation

CCR2CCR5

CCR2CCR5

Kupffer Cell activation

Fat accumulation drives liver injury

CCR2CCR5

Monocyte/macrophage recruitment

NASH Disease Progression

Strong Data Set Supporting CVC in NASH

12

1. Thompson et al. Presented at AASLD 2014; 2. Sherman et al. Presented at HepDart 2015; 3. Lefebvre et al. Presented at AASLD 2014; 4. Lefebvre et al. Presented at AASLD 2013; 5. Friedman et al. Presented at HEP DART 2013; 6. Moyle et al. Presented at AIDS 2014; 7. Tacke et al. Presented at AASLD and Industry Colloquium 2015; 8. Krenkel et al. Presented at EASL 2015; 9. Krenkel et al. Presented at AASLD 2015

Hepatic Impairment Safety Phase 13

600+ Subjects Dosed in Phase 1 and Phase 2

HIV Ph2b: Inflammation and Fibrosis Biomarkers1,2

NASH Mouse Models4

Liver Fibrosis Rat Model5

Kidney Fibrosis Mouse Model6

Reduction in validated markers of:

• Fibrosis (APRI, FIB-4, & ELF)

• Inflammation (sCD14)

Favorable safety and lipid profile

Therapeutic dose established (150 mg once daily)

Once-daily dosing (30-40 hour half-life)

Improvement in fibrosis across models

Improvement in NAFLD Activity Score

Reductions in monocyte-driven inflammation

Hepato-protective effectModels of Inflammation and Liver Injury7—9

ORION Interim Analysis (n=35) Favorable safety profile in NAFL & NASH subjects

Numeric Improvement in metabolic parameters

CVC Shows a Significant Reduction in Fibrosis and NAFLD Activity Score in the MCD Mouse Model

13 Tacke et al. Presented at EASL 2016

SteatosisP = 0.158

Lobular Inflammation

P = 0.077Hepatocyte Ballooning

***NAFLD Activity Score

**

0 0 0 0

1 1

1

2

2 2

3 3 2

4

6

8

Vehicle CVC Vehicle CVC Vehicle CVC Vehicle CVC

Area

frac

tion

%

0.0

0.5

1.0

1.5

2.0

2.5 ns **

**

CVCVhc.8wk.MCD

WTCVCVhc.8wk.MCDWT

0

5

10

15

Live

r Leu

kocy

tes % ns ***

***

Hepatic MoMF% Fibrosis - Sirius Red

Treatment with CVC reduced hepatic macrophages and fibrosis

Treatment with CVC significantly reduced ballooning and NASEASL 2016

CVC Clinical Data

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CVC Normalized Elevated APRI and FIB-4 Scores

15 Friedman et al, Contemporary Clinical Trials 47 (2016) 356–365

Score reduced to <0.5 Score ≥0.5 Score reduced to <1.45 Score ≥1.45

Week 24

Week 48

APRISubjects with Baseline score of ≥0.5

FIB-4Subjects with Baseline score of ≥1.45

75%(12/16)

67%(8/12)

73% (11/15)

71% (10/14)

HIV+ Subjects with paired Baseline and Week 24 and/or 48 data

Non-invasive Tools to Predict Fibrosis Stage

• APRI and FIB-4 are used to predict liver fibrosis in patients with HCV1,2 and NAFLD3,4

• In NASH subjects, early drop in FIB-4 score was significantly associated with fibrosis improvement at 72 weeks5

• From CENTAUR Study Screening Characteristics6…– APRI and FIB-4 scores increased with severity of fibrosis stage

– APRI and FIB-4 cut-offs were identified to reduce the number of nonfibrotic NASH candidates undergoing liver biopsy in Phase 3

• APRI ≥0.53 was predictive of liver fibrosis (Stage 1–4), with a PPV of 92%

• FIB-4 ≥1.11 was predictive of liver fibrosis (Stage 1–4), with a PPV of 88%

161. Lin et al. 2011; 2. de Oliveira et al. 2016; 3. Stal et al. 2015; 4. Morling et al. 2014; 5. Chalasani et al. 2015; 6. Lefebvre, DDW, 2016

CVC Improved Enhanced Liver Fibrosis Scores

17 Sherman KE et al. HEP DART 2015

Baseline Week 48

5

7

9

11

13

15

Baseline Week 48

ELF Index

P < 0.0001 P = 0.6322Not significant

CVC Treatment GroupN=36

Efavirenz Treatment GroupN=16

5

7

9

11

13

15Mean10.53 ± 2.12

Mean 8.28 ± .99

• ELF is a biomarker fibrosis panel consisting of hyaluronic acid, procollagen III N-terminal propeptide and tissue inhibitor of malloproteinases

• Significant decrease in ELF scores observed in CVC treated patients (p< 0.0001)

• No significant change in patients treated with efavirenz (p=0.6322)

FibrosisInflammation

The Molecular Engines that drive NASH

Adapted from Arun Sanyal, NASH Symposium Paris June 2015

Focus of ORION

Focus of CENTAUR

NAFLDNASH

Cirrhosis HCCMetabolic

Abnormality

18

ORION: NAFLD Phase 2a StudyInterim Analysis: potent CCR2/5 antagonism impacts metabolic parameters

19 NCT02217475

Screening liver biopsy

Stratified by presence or absence of NASH

CVC150 mg

Placebo

45 subjects enrolled

Key eligibility criteria

• Adults (18—75 years)

• BMI ≥30 kg/m2• Prediabetes or T2DM

• FPG: 100—270 mg/dL

• HbA1c: 5.7—10.0%• Suspected NAFLD

warranting liver biopsy

Primary endpoint• Change in insulin sensitivity

over 24 weeks of treatment

Secondary endpoints• Measures of

monocyte/macrophage activation and function

• Non-invasive imaging correlated to liver histology

• Fasting metabolic parameters

• Biomarkers of inflammation• Measures of CCR2/CCR5

blockade and receptor occupancy

• Safety & Tolerability

Finalliver biopsyNASH patients

only

PBO Subtracted Interim Results• HbA1c: -0.36 (CI; -0.74, 0.01)• FPG: -11.52 mg/dL (CI; -28.35, 5.31)• FFA (AUC-2h): -4.9 mmol/L (CI; -

11.4, 1.6)

Primary (Week 24)Baseline

Interim(Week 12)

Rand

omiza

tion

1:1

20

CENTAUR Phase 2b Study

CENTAUR: NASH with Fibrosis Phase 2b Study

21Friedman et al, Contemporary Clinical Trials 47 (2016) 356–365NCT02217475

Primary endpoint biopsy

Baselinebiopsy

Year 2 (Q3 17)

Year 1 Primary

(Q3 16)

CompletedEnrollment

(June 15)

Year 2biopsy

Enrolled 289 subjects

Global study

Key eligibility criteria

• Biopsy diagnosis of NASH with fibrosis

• Enriched for patients with• T2DM

• high BMI with >1 criteria of metabolic syndrome

• bridging fibrosis and/or definite NASH

50% placebo assigned to CVC 150mg during

Year 2

Primary endpoint2-point improvement in NAS without worsening of fibrosis

Key secondary endpointResolution of NASH without worsening of fibrosis

Other endpoints• Improvement in fibrosis stage • Collagen morphometry• α-SMA, CK-18• Validated fibrosis scores• Noninvasive imaging

biomarkers• Kidney function

CVC 150 mg(Arm A)

Placebo(Arm B+C)

Rand

omiza

tion

1:1

CENTAUR Exclusively Enrolled Adults at Increased Risk of Progression to Cirrhosis

Friedman et al. Poster 95 presented at HEP DART 2015, December 6–10 2015, Grand Wailea, HI, USA

The majority of CENTAUR patients have NAS ≥5 (74%) and moderate-to-bridging fibrosis (67%), where placebo response is lowest in previous studies

NAS 630%

% Subjects by NAS % Subjects by Fibrosis Stage(NASH CRN)

NAS 530%

NAS 426%

NAS 712%

NAS 82%

F338%

F229%

F133%

22

23

EVO for NASH

The Molecular Engines that Drive NASH

24 Adapted from Arun Sanyal, NASH Symposium Paris June 2015

Fibrosis

NAFLDNASH

Cirrhosis HCCMetabolic

Abnormality

CenicrivirocTargets inflammation

and fibrogenesis

EvogliptinTargets metabolic

abnormalities

Inflammation

Dipeptidyl Peptidase-4 (DPP-4) Inhibition

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• Widely used class for the treatment of Type 2 Diabetes

• Systemically, DPP-4 inhibition results in GLP-1 mediated hypoglycemia and other beneficial effects relevant to the NASH population including1:–Delayed gastric emptying

– Increased satiety

– Increased glucose-dependent insulin secretion

–Decreased glucagon secretion

– Improved beta cell function

• DPP-4 is highly expressed in the liver and plays a direct role in:–Regulation of hepatic gluconeogenesis2,3

–Regulation of lipid metabolism4-6

• In NASH, increased DPP-4 serum levels and hepatic DPP-4 expression is correlated with disease severity2,7,8,

• In preclinical and clinical settings, DPP-4 inhibition has been shown to:–Decrease hepatic glucose production10-12

– Improve hepatic triglyceride content and steatosis4,12-16

–Reduce histologic markers of inflammation and ballooning12-17

Systemic Effect Liver Specific

1. Pharmacotherapy 20102. Miyazaki M, et al 20113. Omar et al 20144. Macauley et al, 2015

5. Kishitani et al, 20146. Monami et al, 20127. Firneisz et al, 20108. Balaban YH et al 2007;

13. Shirakawa J et al. 201114. Klein et al, 201315. Jung et al, 201516. Ideta et al, 2016

9. Solis-Herrera et al, 201310. Kern et al, 201211. Lu et al, 201212. Yilmaz Y et al. 2012

17. Kanazawa et al, 2014

Evogliptin Overview

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• Oral, once daily 5mg tablet

• Potent and reversible DPP-4 inhibition with high selectivity

– Same DPP-4 class as sitagliptin

• Approved in 2015 in Korea for Type 2 Diabetes Mellitus*

– Tested in over 750 patients

– Evaluated in monotherapy and in combination with metformin in Phase 3 Studies

– Comparable efficacy and safety to sitagliptin (Januvia)

*Not approved in US1. C. F. Deacon & H. E. Lebovitz, 20162. Nabeno et al, 20133. Kushwaha et al, 2014

Brand Name (Korea) Suganon® (Evogliptin)

Dose 5mg once dailySingle tablet

Half-life 32-39h

Hepatic Metabolism No clinically meaningful metabolites

Dose adjustment inrenal impairment1

No

Co-Administration with CYP3A4 inducers

Yes

IC50 in Human Plasma 7.5 nM

DPP-4 Subsite Binding2,3

S2 Extensive S2 S1 S1’ S2’

EvogliptinSitagliptin

Saxagliptin/VildagliptinAlogliptin/Linagliptin

Transaction Overview

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Product Evogliptin to Tobira Cenicriviroc to Dong-A

Territory United States, Canada, Europe, Australia South Korea

Field of Use All indications All indications

Economics • Upfront - $1.5M

• Up to $25 million in payments linked to the achievement of Phase 3 completion and regulatory approvals and $10 million for additional indications.

• Up $35 million in commercial milestones and tiered royalty payments based on net sales

• Upfront - $0.5M

• Up to $2.5 million in payments linked to the achievement of development andcommercial milestones

• Tiered royalty payments based on net sales

Planning for CVC + EVO in clinic in 2016

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CVC for Primary SclerosingCholangitis

Primary Sclerosing Cholangitis (PSC)

• Chronic cholestatic disease affecting bile ducts– Progresses to cirrhosis over 10-15 years

– 10-15% develop cholangiocarcinoma

• U.S. prevalence 44,000; 60-80% concomitant IBD– Age at diagnosis: 41 years old (symptomatic)

– Treatment is Liver Transplant; No approved drug

• CCL2 plays a key role in PSC• Genetic data suggest important role of CCR5

– CCR5-Δ32 is protective for PSC1

– CCL5 promoter-activating mutation is associated with PSC2

• CVC differentiation– Potentially disease modifying

– Suitable for chronic administration (oral, QD, well-tolerated)

1. Henckaerts Inflamm. Bowel Dis. 2006; 4 272; Eri Genes Immun. 2004; 5 444;Tissue Antigens 2006; 68 782. Henckaerts Gut 2007; 56 89129

CX3CR1CC

R2

51%

PERSEUS – PSC Proof of Concept Study Design

CVC 150 mg

25 subjects

7-10 centers (US & CA)

Key eligibility criteria• Adult with large duct PSC

• Serum ALP ≥ 1.5 times ULN

• Confirmed IBD

• Non-cirrhotics

Primary endpointChange from baseline in serum ALP through Week 24

Other analyses:• Proportion of subjects

achieving:• ALP normalization• <1.5 x ULN • 50% decrease in ALP

• Hepatic biochemistries• Fibroscan• Safety/tolerability• Mayo IBD Score

Primary (Week 24)Baseline

Week 12Analysis

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Summary

31

• Initiate Phase 3 NASH program

• PERSEUS Phase 2 data readout

• Initiate CVC + EVO Phase 2

• CENTAUR primary endpoint (Q3)

• Finalize Phase 3 design (Q4)

• CVC + EVO Phase 1 (Q4)

Initiate proof of concept clinical study in PSC

Initiate NASH combination programs

ORION Phase 2a interim data

Complete Phase 3 enabling studies

Building Value

32

H12016

H22016

2017

Changing the Course of NASH & Liver Disease

33

Building a leading NASH program• Cenicriviroc (CVC) Phase 2b CENTAUR data Q3 2016• Evogliptin (EVO) + CVC combination study planned for 2016

Building long-term value• Transition to Phase 3 for CVC single-agent, combinations to follow• Q1 2016 cash balance: $53 million; cash runway to H2 2017

CVC: potent immuno-inflammatory agent• Once-daily dosing & favorable safety profile; cornerstone potential for NASH• Phase 2 in Primary Sclerosing Cholangitis: potential to be disease modifying

T A R G E T I N G S E R I O U S D I S E A S E S O F I M M U N O - I N F L A M M A T I O N A N D F I B R O S I S

Company Contact:Ian Clements, PhDiclements@tobiratx.com

www.tobiratx.com

©2016 Tobira Therapeutics, Inc. All rights reserved. Tobira® is a trademark or registered trademarks of Tobira Therapeutics, Inc. in the United States and other countries. All other trademarks are the property of their respective owners. The information herein is for informational purposes only and represents the current view of Tobira Therapeutics, Inc. as of the date of this presentation. Tobira cannot guarantee the accuracy of any information provided after the date of this presentation. Tobira makes no warranties, express, implied or statutory, as to the information in this presentation.

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