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HCV: Stemming the Tidal Wave
R. Logan Faust, MD, FACGCalifornia Association for Nurse Practitioners Symposium, October
2014
Timeline-Hepatitis C1973: First named non-A, non-B hepatitis
1989: Hepatitis C Genome is cloned; single stranded RNA in the Flaviviridae family.
1989: HCV antibody test is developed
1990: HCV viral load test is developed to detect HCV RNA in serum (PCR)
1998: Combination therapy with interferon and ribavirin is approved by the FDA.
2001: Pegylated interferon is approved by the FDA
2013: Sofosbuvir/Ribavirin is approved by the FDA
2014: Sofosbuvir/Ledipasvir is approved by the FDA
The Numbers
The Numbers
Baby Boomers (Born in 1945–1965)
Account for 76.5% of HCV in the US1
Estimated Prevalence by Age Group2
Birth Year Group
0
1.6
1.4
1.2
1.0
0.8
0.6
0.4
0.2
1990+1980s1970s1960s1950s1940s1930s1920s<1920
Nu
mb
er
wit
h c
hro
nic
HC
V (
mil
lio
ns
)
An estimated 35% of undiagnosed baby boomers with HCV currently have advanced fibrosis (F3-F4; bridging fibrosis to cirrhosis)3
1. Centers for Disease Control and Prevention. MMWR. 2012;61:1-32; Adapted from Pyenson B, et al. Consequences of Hepatitis C Virus (HCV): Costs of a baby boomer Epidemic of Liver Disease. New York, NY: Milliman, Inc; May 18, 2009. http://www.milliman.com/expertise/healthcare/publications/rr/consequences-hepatitis-c-virus-RR05-15-09.php Milliman report was commissioned by Vertex Pharmaceuticals; 3. McGarry LJ et al. Hepatology. 2012;55(5):1344-1355.
7
• An estimated 4 million people are infected excluding the institutionalized populations like the US military and prisons, and an estimated 12 million illegal immigrants
• 40-60% of Chronic liver disease in the US is related to chronic hepatitis C infection
• Chronic HCV is the leading cause of adult liver transplantation
• Between 24,000 to 30,000 deaths yearly associated with chronic liver disease related to chronic HCV *
• Approximately 80% of people who become infected with the hepatitis C virus develop chronic infection
• In 2011, the estimated economic burden associated with chronic HCV infection in the US was $6.5 billion.
US Disease Prevalence & Burden
Adapted from Reindollar RW, Am J Med, 1999.
Worldwide prevalence of HCV in correctional populations
Projected Numbers of Decompensated Cirrhosis and Cases of HCC to Rise Through
2020
10
Incidence of HCC in the United States
Altekruse SF, et al. J Clin Oncol. 2009;27:1485-1491. Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
Year
Incid
en
ce R
ate
9
8
7
6
5
4
3
2
1
0
10
1975 1980 1985 1990 1995 2000 2005
Men
Overall
Women
Deaths Due to HCV Infections Now
Exceed Those Due to HIV Infection
Ly KN et al. Ann Intern Med. 21 February 2012;156(4):271-278; Mahajan, IDSA 2013
15,106
12,734
Number of HCV-related deaths may be over 60,000 because of
under-reporting on death certificates
12
Complications of Advanced Liver
Disease Clinical
Portal hypertension Thrombocytopenia, varices, nodular liver, enlarged spleen
Impaired hepatic function Albumin, bilirubin, INR
Decompensation: advent of complications Ascites Encephalopathy Variceal hemorrhage Jaundice Cancer
Sangiovanni A, et al. Hepatology. 2006;43:1303-1310.
Survival Probability in HCV Patients
With Cirrhosis
Reprinted from Gastroenterology, 112, Fattovich G, et al, Morbidity and mortality in compensated cirrhosis type C: A retrospective follow-up study of 384 patients, 463-472., Copyright 1997, with permission from Elsevier. http://www.sciencedirect.com/science/journal/00165085.
Compensated
After first major complication
Survival Probability100
Pati
en
ts (
%) 80
60
40
20
0120
0 12 24 36 48 60 72 84 96 108Mos
QoL Reductions in HCV-Infected Pts
Without Significant Liver Disease
Systematic review of 15 studies comparing QoL in patients with compensated HCV vs healthy controls
HCV may diminish QoL in the absence of clinically significant liver disease through extrahepatic somatic symptoms, extrahepatic disorders, or cognitive dysfunction
Weig
hte
d M
ean
C
han
ge in
SF-3
6
Score -7.0
15
5
20
10
Physical
Function
Role, Physica
l
Bodily Pain
General
HealthVitality
Social Functio
n0
Role, Emotion
al
Mental Health
25
-15.8
-9.0-12.6
-10.1 -11.9-13.0
-7.2
Spiegel BMR, et al. Hepatology. 2005;41:790-800.
Burden of disease related to
HCV
Sou
rce: W
HO
Hep
atitis C
t S
heet h
ttp://w
ww
.wh
o.in
t/imm
un
izati
on
/top
ics/hep
atitis_c/e
n/in
dex.h
tml
Outcome Key Facts
Cirrhosis• Develops in 20-30% of those who are
chronically infected with HCV over 20-30 years
Decompensated Cirrhosis
• High risk of mortality from ruptured esophageal varices, bacterial peritonitis, hepatorenal syndrome/renal failure, encephalopathy
Hepatocellular Carcinoma
• Fastest growing Cancer in the US • 76% associated with chronic HCV
infection• 4% annual incidence in those with
cirrhosis
Liver Transplantation • HCV responsible for 65% of liver transplants worldwide
HCV Mortality • Estimated at 16,000/year• Likely to peak ~2030
45%may never develop se-
rious liver damage47% may develop mild to moderate liver damage
7%may develop
cirrhosis
1% may develop
liver failure or cancer
Of 100 people with chronic hepatitis C who remain untreated af-ter 20 years
Natural History
Serum ALT Levels: An Imperfect
Marker of Liver Disease Severity Distribution of hepatic fibrosis in 95 HCV-infected patients
0
20
40
60
80
100
No fibrosis Mild BridgingPortal
Severity of Liver Disease
Pati
en
ts (
%)
Normal ALTElevated ALT
2319
39
1926 24
616
Cirrhosis
6
22
Shiffman ML, et al. J Infect Dis. 2000;182:1595-1601.
Serum HCV RNA Does Not Correlate
With Level of Inflammation
Inflammation Score
Genotype
1
2
3
4
0
2
4
6
8
Log
HC
V R
NA
(cop
ies/m
L)
20 4 6 8 10 12
Ferreira-Gonzalez A, et al. Use of Diagnostic Testing for Managing Hepatitis C Virus Infection. Semin Liver Dis. 2004;24(Suppl 2):9-18. Reprinted by permission.
Serum HCV RNA Does Not Correlate
With Level of FibrosisGenotype
NoFibrosis
PortalFibrosis
BridgingFibrosis
Cirrhosis
0
2
4
6
8
Log
HC
V R
NA
(cop
ies/m
L)
1
2
3
4
Ferreira-Gonzalez A, et al. Use of Diagnostic Testing for Managing Hepatitis C Virus Infection. Semin Liver Dis. 2004;24(Suppl 2):9-18. Reprinted by permission.
HCV RNA Testing Has No Prognostic Value:
The level of viremia does not correlate with the severity of liver disease (activity grade or fibrosis stage)
Does not predict the outcome of HCV infection (resolution vs. persistence)
Does not predict the natural course of the disease
Alcohol Consumption Increases Risk
of Cirrhosis in HCV Patients
*Excessive alcohol intake characterized as > 40 g/day for women and > 60 g/day for men.†Duration of exposure defined as either first blood transfusion before 1990 or from the year of initial intravenous drug use.
0
20
40
60
80
100
10 20 30 40Years Following Exposure†
Cir
rhosis
(%
)
HCV
HCV + alcohol*
Wiley TE, et al. Hepatology. 1998:28:805-809.
6
1812
58
31
64
40
85P < .01 P < .01
P < .01
SVR (Cure) Associated with
Decreased All-Cause Mortality 10
-yea
r C
umul
ativ
e In
cide
nce
Rat
e
530 patients with advanced fibrosis, treated with interferon-based therapy, and followed for 8.4 (IQR 6.4-1.4) years
Van der Meer et al. JAMA 2012; 308:2584
8.9
26
5.1
21.8
2.1
29.9
24
Improvement in Fibrosis at Week 72
Following Start of HCV Therapy
Pati
en
ts W
ith
Im
pro
vem
en
t in
Fib
rosis
≥ 1
Sta
ge (
%)
Mean
Fib
rosis
Ch
an
ge
(Meta
vir
Sta
ge)
Everson GT, et al. Aliment Pharm Ther. 2008;27:542-551.
Varied With Response to Treatment
-1.2
-1.0
-0.8
-0.6
-0.4
-0.2
0SVR Relapse NR
0
10
20
30
40
50
60
SVR Relapse NR
70
80
90
100
What do we get with HCV
treatment?
Lok A. NEJM 2012; Ghany M. Hepatol 2009; Van der Meer AJ. JAMA 2012
SVR (cure) of HCV is associated with: 70% Reduction of Hepatocellular
CA50% Reduction in all-cause
mortality90% Reduction in Liver Failure
??
Progression of HCV Liver Disease:
Summary Chronic HCV infection leads to cirrhosis and liver failure in
a large number of persons Clinical complications of advanced liver disease include portal
hypertension, ascites, variceal bleeding, and HCC
Rates of progression dependent on modifiable and nonmodifiable factors
Effective treatment of chronic HCV infection can prevent fibrosis progression and reduce complications of HCV Treatment outcomes impacted by baseline fibrosis and
cirrhosis
The best way to reduce the
likelihood that someone will develop
severe complications of hepatitis C is
to cure the infection
28
Adapted from the US Food and Drug Administration, Antiviral Drugs Advisory Committee Meeting, April 27-28, 2011, Silver Spring, MD.
SV
R (
%)
IFN6 mos
PegIFN/ RBV
12 mos
IFN12 mos
IFN/RBV12 mos
PegIFN12 mos
2001
1998
2011
StandardIFN
RBV
PegIFN
1991
DAAs
PegIFN/RBV/DAA
IFN/RBV6 mos
6
16
3442 39
55
70+
0
20
40
60
80
100
DAA + RBV
± PegIFN
90+
2013
The Good News
Falck-Ytter, Y. Annals, 2002.
Why do we need IFN-free
regimens?Efficacy
Poorly interferon responsive African Americans Prior IFN failure
Null responder cirrhotics
Acceptance and tolerability
Poor patient acceptance
Providers reluctance Resource intensive
Monitoring: toxicity Support services
Interferon ineligible populations
Decompensated ESLD
Severe psychiatric disease
Medical co-morbidities
100 HCV RNA+ Patients
40 Eligible Patients
5 Cured
30% refusal
75% dropout or nonrespon
se
60% Ineligibl
e
28 Treated
HCV Life Cycle and DAA Targets
Adapted from Manns MP, et al. Nat Rev Drug Discov. 2007;6:991-1000.
Receptor bindingand endocytosis
Fusion and
uncoating
Transportand release
(+) RNATranslation
andpolyprotein processing
RNA replication
Virionassembly
Membranousweb
ER lumen
LD
LDER lumen
LD
NS3/4 protease inhibitors
NS5B polymerase inhibitors
Nucleoside/nucleotide
Nonnucleoside
Block replication complex formation, assembly
NS5A inhibitors
RNA replication
Not All Direct-Acting Antivirals are
Created Equal
Characteristic Protease Inhibitor*
Protease Inhibitor**
NS5AInhibitor
Nuc Polymerase
Inhibitor
Non-NucPolymerase
Inhibitor
Resistance profile
Pangenotypic efficacy
Antiviral potency
Adverse events
Good profile Average profile Least favorable profile
*First generation. **Second generation.
The First DAAs:Telaprevir and
Boceprevir
A Major Advance:
GT1 Treatment-Naïve Patients
0
20
40
60
80
100SV
R (
%)
PegIFN/RBV BOC or TVR + PegIFN/RBV
38-44
63-75
Poordad F, et al. N Engl J Med. 2011;364:1195-1206. Jacobson IM, et al. N Engl J Med. 2011;364:2405-2416.
A Major Advance:
GT1 Treatment Failures
0
20
40
60
80
100
SV
R (
%)
Relapsers[1,2] Partial Responders[1,2]
69-83PegIFN/RBV
1. Bacon BR, et al. N Engl J Med. 2011;364:1207-1217. 2. Zeuzem S, et al. N Engl J Med. 2011;364:2417-2428. 3. Bronowicki JP, et al. EASL 2012. Abstract 11.
NullResponders[2,3]
BOC or TVR + PegIFN/RBV
24-29
40-59
7-15
29-40
5
No Free Lunch
Treatment is more effective but much more difficult
Other Issues With PI-Based Therapy
Pill burden Food requirement
CYP3A4PI metabolites
Drug-drug interactions
Resistance
BOC = 12/dayRBV = 4-7/day
TVR = 6/dayRBV = 4-7/day
Progress Has Not Been Linear
Tolerability/Safety
Effi
cacy
Peg/RBV
Peg/RBV+ BOC/TVR
Peg/RBV+ 2nd-gen DAA
IFN-freeDAA combo
IFN-freeDAA combos
Peg/RBV+ 2 DAAs
1 pill, QD,
No AEs,
100% SVR
Perfectovir
Expectations for New Regimens
Tolerability/Safety
Effi
cacy
Peg/RBV
Peg/RBV+ BOC/TVR
Peg/RBV+ 2nd-gen DAA
Expectations
70% to 80% SVR
QD/BID dosing
Few/no additional AEs
Shorter duration with or without RGT
12-24 weeks for most/all patients
SMV + P/R in GT1 Treatment-Naive
Patients/Relapsers
100
80
60
40
20
0
SV
R1
2 (
%)
80
50
210/
26465/130
81
209/
257
50
67/134
QUEST-1[1] QUEST-2[2]
100
80
60
40
20
0
SV
R1
2 (
%)
79
37
206/
26049/133
PROMISE[3]
Treatment-Naive Patients Prior Relapsers
1. Jacobson I, et al. EASL 2013. Abstract 1425. 2. Manns M, et al. EASL 2013. Abstract 1413. 3. Lawitz E, et al. DDW 2013. Abstract 869b.
P/RSMV + P/R
QUEST Studies: Subtype 1a ≠ 1b
Jacobson I, et al. AASLD 2013. Abstract 1122.
Likely relates to presence of Q80K polymorphism in GT1a
62/131
191/254
70/133
228/267
SV
R1
2 (
%)
100
80
60
40
20
0GT1a GT1b
Simeprevir + P/R (RGT 12 + 12)
Placebo + P/R75
47
85
53
Summary of New PIs + P/R in GT1
HCV: Simeprevir and Faldaprevir
Pros Once-daily PI Well tolerated with less rash and no anemia > 85% of patients shorten treatment duration
to 6 months and most achieve SVR
Cons Q80K major issue with SMV; pretreatment
testing required in all GT1a patients considered for SMV
DDIs still an issue (SMV > FDV) Must be combined with P/R
NEUTRINO: Sofosbuvir + P/R for 12
Weeks in Treatment-Naive GT 1/4/5/6
HCV Open-label, single-arm study of sofosbuvir 400 mg QD + P/R
for 12 weeks in treatment-naive patients with GT1/4/5/6 HCV 17% cirrhosis; 89% GT1; 9% GT4; < 1% GT5; 2% GT6
Lawitz E, et al. N Engl J Med. 2013;368:1878-1887.
Overall
SV
R1
2 (
%)
8996
100100
80
60
40
20
0GT1 GT4 GT5,6
261/292
27/28 7/7n/N =
90
295/327
92
80
100
80
60
40
20
0No
CirrhosisCirrhosis
252/273 43/54
Summary of Sofosbuvir + P/R in GT1
HCV
Pros Once-daily nucleotide polymerase inhibitor Very well tolerated Given for only 12 weeks in all GT1 patients (no
RGT) High SVR even in cirrhosis (80%) Same regimen approved for GT4
Cons No control group for GT1 Insufficient data for GT5,6 But data are hard to argue with—very promising
Lawitz E, et al. N Engl J Med. 2013;368:1878-1887.
Examples of IFN-Free DAA Combinations
Tolerability/Safety
Effi
cacy
Peg/RBV
Peg/RBV+ BOC/TVR
Peg/RBV + 2nd-gen DAA
IFN-freeDAA combos
PI +
Nuc +
96
Example of Nuc Backbone + PI in
Trt-Naive Pts and Nulls (COSMOS)
SV
R1
2 (
%)
F0-F2 Fibrosis
100
80
60
40
20
0
96 93
26/27
13/14
SMV (PI) + SOF (Nuc) + RBV 12 wks SMV (PI) + SOF (Nuc) 12 wks
SV
R4
(%
)
F3/F4 Fibrosis
100
26/27
14/14
78% GT1a
50% Q80K
All nulls
78% GT1a
40% Q80K
47% F4
54% Null
Jacobson I, et al. AASLD 2013. Abstract LB-3.
Major caveats: small n, no plan for phase III trial
1-Pill Version of Nuc + NS5A
Treatment-naive patients (noncirrhotic)
SV
R4
or
12
(%
)
95
19/20
100
21/21
SOF/LDV SOF/LDV + RBV
8 wks
95
18/19
SOF/LDV
18/19
95
21/21
100
SOF/LDV+ RBV
SOF/LDV
12 wks
PI failures (50% cirrhotic)
12 wks
No breakthrough; 2 relapses, both without RBV 1 case of resistance – retreated with SOF/LDV + RBV x 24 weeks → SVR
Lawitz E, et al. AASLD 2013. Abstract 215.
LONESTAR: SOF (Nuc) + ledipasvir (NS5A) FDC ± RBV
100
80
60
40
20
0
Phase III Studies of Sofosbuvir (Nuc) +
Ledipasvir (NS5A) ± RBV in GT1 HCVION-1*: GT1 treatment-
naive pts (16% cirrhotic): SOF/LDV FDC ± RBV for 12
wks
Press release. These data are available in press release format only, have not been peer reviewed, may be incomplete, and we await presentation or publication in a peer-reviewed format before conclusions should be made from these data.
*24-wk arms not yet reported.
ION-3: GT1 treatment-naive pts: SOF/LDV FDC ± RBV
for 8 or 12 wks
SOF/LDV FDC SOF/LDV FDC + RBV
ION-2: GT1 treatment-experienced pts (20% cirrhotic): SOF/LDV FDC ± RBV for 12 or 24
wks
8 Wks 12 Wks
202/215
206/216
201/216
12 Wks 24 Wks
102/109
107/111
108/109
110/111n/N =
209/214
211/217
SV
R1
2 (
%)
12 Wks
98 97100
90
60
40
20
0
94 93 95 94 96 99 99
What About Resistance?
Lawitz E, et al. AASLD 2013. Abstract 215.
7
6
5
4
3
2
0HC
V R
NA
(lo
g1
0 IU
/mL)
SOF/LDV8 Wks
Post-treatment
Retreatment:SOF/LDV + RBV
24 Wks
Post-treatment
SVR12
HCV DETHCV ND
NS5A:L31M (94.38%)
NS5B:S282T (8.00%)
NS5A:L31M (> 99%)
NS5B:S282T (91.24%)
NS5A:L31M 25.5%NS5B:No RAVs
What about GT2 and GT3?
FUSION: SVR by GT and Cirrhosis in
Treatment-Experienced Patients
Jacobson IM, et al. N Engl J Med. 2013;368:1867-1877.
Sofosbuvir + RBV 12 wks
Sofosbuvir + RBV 16 wks100
12 weeks sufficient for GT2 16 weeks better than 12 weeks for GT3… so what about 24
weeks?
5/26
SV
R1
2 (
%)
25/26
23/23
14/38
14/23
25/40
No Cirrhosis No CirrhosisCirrhosis CirrhosisGT2 GT3
19
6163
37
n/N =
100
80
60
40
20
0
9688
100
80
60
40
20
0
SV
R1
2 (
%)
Treatment Naive[1]
Treatment Experienced[1]
SV
R1
2 (
%)
n/N =12/13
87/100
100
80
60
40
20
0
94 9287
86/92
27/45
60
No Cirrhosis
1. Zeuzem S, et al. AASLD 2013. Abstract 1085. 2. Jacobson IM, et al. N Engl J Med. 2013;368:1867-1877.
VALENCE: Efficacy With 24-Week
Sofosbuvir Plus Ribavirin in GT3
Patients
14/23
FUSION[2] Cirrhosis
24 weeks better for treatment-naive patients
Not ideal for cirrhotic treatment failures
SV
R1
2 (
%)
n/N =
100
80
60
40
20
0
61
24 Wks 24 Wks 16 Wks
Do We Still Need IFN for GT3?
Lawitz E, et al. AASLD 2013. Abstract LB-4.
100
80
60
40
20
0
SV
R1
2 (
%)
100
9/9
83
10/12
GT 2 GT 3
93
13/14
No cirrhosis
Cirrhosis83
10/12
85% previous treatment failures
LONESTAR-2: SOF + PegIFN + RBV x 12 wks
Small single-center study but looks promising. . .
IFN is not dead yet!
Will There Still Be a Role for IFN?
Hard to cure GT3, treatment experienced, cirrhosis DAA failures – multi-DAA resistant Prior nonresponders → Quad?
Cost containment Fewer or less effective DAAs GT2?
FISSION: Better Tolerability Profile
With Sofosbuvir/RBV vs PegIFN/RBV Grade ≥ 3 AEs: 7% with SOF/RBV vs 19% for pegIFN/RBV
Discontinuations due to AEs: 1% for SOF/RBV vs 11% for pegIFN/RBV
Gane E, et al. EASL 2013. Abstract 5.
GT2/3 Pts, AEs Occurring in ≥ 15% in Either Arm, %
SOF/RBV(n = 256)
PegIFN/RBV(n = 243)
P Value
Fatigue 36 55 < .0001
Headache 25 44 < .0001
Nausea 18 29 .0057
Insomnia 12 29 < .0001
Rash 9 17 .0052
Diarrhea 9 17 .0075
Irritability 10 17 .0328
Decreased appetite 7 18 .0001
Myalgia 8 17 .0060
Pruritus 7 17 .0009
Influenzalike symptoms 3 18 < .0001
Chills 3 18 < .0001
Sofosbuvir + RBV for Special
Populations:
Approved Indications
Sofosbuvir + RBV for treatment of patients with HCC awaiting liver transplantation for up to 48 weeks or until liver transplantation, whichever occurs first
For HIV/HCV-coinfected patients, sofosbuvir should be administered according to HCV genotype No differences between monoinfected and coinfected
patients
Sofosbuvir [package insert]. December 2013.
Duration of Undetectable HCV RNA
Before Transplantation Predicts Lack of
Recurrence
Curry MP, et al. AASLD 2013. Abstract 213.
3300 30 60 90 120 150 180 210 240 270 300
Days With HCV RNA Continuously TND Before Liver Transplantation
> 30 days HCV (-)
No recurrence (n = 28)Recurrence (n = 10)
Median days undetectable (P < .001) No recurrence: 95 Recurrence: 5.5
Only 1 of 24 patients with undetectable HCV RNA > 30 days experienced recurrence
Sofosbuvir + RBV ± PegIFN in Post-LT
HCV: Virologic and Safety Outcomes
69% of patients had SVR4; 56% had SVR12 2/36 patients relapsed 1/36 patients had on-
treatment nonresponse 8/36 patients died
64% of patients showed improvement of decompensation events
11% of patients showed stabilization of events
Forns X, et al. AASLD 2013. Abstract 1084.
Overall SOF + RBV
SOF +PegIFN/RBV
SV
R4
(%
)
100
80
60
40
20
0
6974
56
25/36 20/27 5/9n/N =
Early Results in Coinfected
Patients
n/N =
1. Sulkowski M, et al. AASLD 2013. Abstract 212. 2. Rodriguez-Torres M, et al. IDSA 2013. Abstract 714. 3. Rockstroh JK, et al. AASLD 2013. Abstract 1099. 4. Dieterich D, et al. EACS 2013. Abstract LBPS9/5. 5. Jacobson I, et al. EASL 2013. Abstract 1425.
100
80
60
20
0
40
SV
R1
2 (
%)
GT1: SOF+ RBV for 24 wksGT2: SOF + RBV for 12 wksGT3: SOF + RBV for 12 wks
76
88
67
87/114
23/26
28/42
PHOTON-1[1]
The Final Word
Genotype 1, single daily tablet
Treatment naïve with or without cirrhosis:12 weeks*
Treatment experienced without cirrhosis:12 weeks
Treatment experienced with cirrhosis:24 weeks
sofosbuvir 400mg/ledipasvir 90mg (Harvoni)
The Final Word
Genotype 2, two/three pills bid
Treatment naïve with or without cirrhosis:12 weeks
Treatment experienced without cirrhosis:12 weeks
Treatment experienced with cirrhosis:12 weeks*
sofosbuvir 400mg/ribavirin 1000-1200mg (Solvadi/Ribavirin)
The Final Word
Genotype 3, two/three pills bid
Treatment naïve with or without cirrhosis:24 weeks
Treatment experienced without cirrhosis:24 weeks
Treatment experienced with cirrhosis:24 weeks
sofosbuvir 400mg/ribavirin 1000-1200mg (Solvadi/Ribavirin)
The Final WordGenotype 1, 8 weeks, $63,000
12 weeks, $94,500 24
weeks, $189,000
Genotype 2, 12 weeks, $84,000
Genotype 3, 24 weeks, $168,000
“If we treated 26 patients, that would be equivalent to our entire drug budget for the county jail system — for everybody — for a year,” said David Woods, the chief pharmacy officer of San Francisco’s Public Health Department