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