HCV: The next 18 months. David L. Wyles, M.D. Associate Professor of Medicine UCSD

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Transcription:

HCV: The next 18 months David L. Wyles, M.D. Associate Professor of Medicine UCSD

FIRST, A LOOK BACK WHAT DID I SAY LAST YEAR?

My predictions for genotype 1: Multiple highly efficacious, well-tolerated, IFNfree genotype 1 regimens will be approved SOF+NS5A: no RBV; 8 weeks naïve, 12 weeks all others SOF/DCV compassionate use right now in EU SOF/PI: as efficacious; no phase 3 planned PI-based regimen(s): RBV for some (1a); 12 weeks ± Similar efficacy Prior PI failures Slightly more complex dosing Drug interaction potential Almost no role for Interferon from a medical standpoint ±?

Closing Remarks (2014) Progress on HCV antiviral continues at a remarkable pace Multiple IFN-free regimens with >95% SVR rates will be approved for GT1 Promising option for difficult to treat GT3 cirrhotics exist but more data is needed Resistance will not be major consideration Challenges facing us include diagnosis, access to care (providers), and resource allocation

Outline: The next 18 months Evolution of GT1 therapy yawn. Approval of additional regimens Non-genotype 1 and pangenotypic regimens This is where the action is! The race to shorten therapy Is it worthy of all the hype? Is resistance dead? The emergence of NS5A resistance

NEW REGIMENS FOR GENOTYPE 1

C-WORTHY Studies Grazoprevir- next generation NS3 PI Enhanced pangenotypic activity Higher resistance barrier Elbasvir- NS5A inhbitor Potent, pangenotypic activity GZP 100mg + ELB 50mg +/-RBV Non-cirrhotic: 8 wks vs 12 wks 59% male, 88% white, 73% 1a, 8% F3 Included HIV co-infected subjects Null and/or Cirrhosis: 12 wksvs18 wks Sulkowski MS. Lancet 2014. Lawitz E. Lancet 2014.

C-WORTHY Non-cirrhotic 100 80 80 92 95 95 92 SVR12 (%) 60 40 All 1a 1b 20 0 30 52 22 76 36 8 wks + R 12wks 12wks + R 4% virologic failure rate in 12 week arms (7/188). Sulkowski MS. Lancet 2014.

C-WORTHY Difficult to treat populations 100 80 97 94 90 91 94 97 97 100 100 80 Null Cirrhotics 92 100 60 60 40 40 20 20 0 12 wks 12wks + R 18wks 18wks + R 0 25 23 12 weeks 18 weeks Naïve Cirr Null +/- Cirr Lawitz E. Lancet 2014.

UNITY-2: BMS Trio Regimen Phase 3 study in naïve (n=112) and experienced (n=90) cirrhotics Trio FDC [DCV 30mg/ASV 200mg/BCV 75mg] BID Compensated cirrhosis (CPT A) Plt>50k (26% of ptswith Plt<100k) INR <1.7 ALB >3.5 TN N=57 TE N=45 Trio TN TE N=55 N=45 Trio + RBV SVR12 0 12 24 Muir A. #LB-2 AASLD 2014.

BMS Trio SVR12 Results 100 80 93 98 87 93 SVR12 (%) 60 40 Trio Trio + R 20 0 TN TE Muir A. #LB-2 AASLD 2014.

SVR12 by genotype 100 80 90 97 Naïve 100 100 80 86 Experienced 91 90 SVR12 (%) 60 40 60 40 Trio Trio + R 20 20 0 1a 1b 0 1a 10 1b Muir A. #LB-2 AASLD 2014.

New regimen approvals for GT1 BMS Trio RBV for all 1a s UNITY-1 (SVR12): 89% 1a vs. 98% 1b PoordadF. AASLD 2014 Do treatment experienced need 24 weeks? Problem: not studied Do TE 1b s need RBV? Grazoprevir/Elbasvir Non-cirrhotic: 12 weeks no RBV Cirrhotics: phase 3 will determine 12 vs. 16 weeks and role of RBV.

What is a truly pan-genotypic regimen? High efficacy across all genoytpes with The same treatment duration No need for RBV for some genotypes Contenders: most are nucleotide + NS5A SOF/GS-5816 SOF/DCV Grazoprevir/Elbasvir The next wave ACH-3102/3422 or ABT-493/ABT-530

Not all NS5A inhibitors are created equal EC50 (pm) 1a 2a 3 4 6 LDV 34 21000 35000 110 120 DCV 50 71 150 12 -- GS-5816 12 9 12 9 6 Elbasvir 4 3 20 3 -- ACH-3102 26 <10x FC in EC50 ABT-530 2 2 2 2 3 Later generation compounds retain activity against variants at polymorphic site (Q30, L31) and those associated with resistance (28, 30, 31, 58, and 93). Wang C. AAC 2012. Zhao Y. #A845 EASL 2012. Ng T. #639 CROI 2014.

ALLY 3 Phase 3 study of SOF/DCV in GT-3 subjects Patients with cirrhosis included TN N=101 TE N=51 SOF/DCV SOF/DCV SVR12 0 12 24 Weeks Nelson DR. # AASLD 2014.

SOF + GS-5816 for GT3 Treatment naïve, non-cirrhotic GT3 SOF + GS-5816 (25 or 100mg) US Study: 12 weeks, no RBV ELECTRON 2: 8 weeks +/-RBV 100 100 93 93 96 100 80 88 60 40 25mg 100mg 20 0 27 27 27 27 27 24 26 12 weeks 8 weeks 8 wk + RBV EversonG. EASL 2014. GaneE. # 79 AASLD 2014.

Great, but We need data in tougher to treat populations Treatment experienced Cirrhosis ALLY-3: Sofosbuvr + Daclatasvir for 12 weeks Only 63% SVR in GT3 cirrhotic patients Studies are ongoing SOF/GS-5816: GT1, 4-6; GT2; GT3 ABT-493/530 in GT2/3 SOF/GZP/ELB in GT3 Nelson DR. #LB-3 AASLD 2014.

The race to shorten therapy. How much does it matter? How short can you go and where are the diminishing returns? Is it worth it if you have a lot of caveats? Fibrosis stage Genotype Viral load Co-infection Etc, etc.

SYNERGY the study that started it all N=20 N=20 SOF/LDV +9669 100 SOF/LDV 9669 9451 N=20 Weeks +9451 6 12 90 80 70 %<LLOQ 60 50 40 30 20 10 0 Week 4 SVR12 KohilA. CROI 2014

SOF/GS-5816 for 8 weeks Treatment naïve, non-cirrhotic patients GT1 N=29 GT2 N=26 SOF/5816 100mg SVR12 GT1 N=31 GT2 N=26 SOF/5816 100mg + RBV 0 12 24 Weeks Tran T. #80 AASLD 2014.

SOF/GS-5816 for 8 weeks 100 80 90 88 81 88 SVR12 (%) 60 40 No RBV RBV 20 0 GT 1 GT 2 14/15 viral failures due to relapse. Tran T. #80 AASLD 2014.

C-SWIFT Study Triple combination of SOF + GZP/ELB Naïve, GT 1 subjects Non-cirrhotic: 4 or 6 weeks Cirrhosis: 6 or 8 weeks 100 80 87 80 95 28/102 (27%) with relapse SVR8 (%) 60 40 40 30% relapse in 1a 20 17% relapse in 1b 0 4 wks 6 wks 6 wks 8 wks Non-cirrhotic Cirrhosis Lawitz E. #LB-33 AASLD 2014.

Summary We are not there yet with DAAs in phase 3 for a truly pan-genotypic regimen Particularly for tough to treat populations GT3 cirrhosis Shortening therapy is nice but should not be priority Below 8 weeks significant drop off occurs Subgroups become more important again! There is a physiologic limit Cost benefits are lost

NS5A RESISTANCE: CLINICAL SIGNIFICANCE?

NS5A resistance background Genotype 1 Similar resistance pattern for 1 st gen NS5A 1a: Q30E/K/R, L31M/V, Y93H/C 1b: L31M/V + Y93H ~15% with baseline RAVs 1a: Q30R/H 1b: L31M/V, Y93H Selected RAVs are relatively fit and persist 86% (63/73 1a) and 95% (56/59 1b) by population Reddy KR. #1965 AASLD 2014.

Impact of NS5A baseline resistance is contextual IFN vsifn-free Strength of surrounding DAAs 38% SVR12 in ASV/DCV with baseline NS5A RAVs (compared to 85% overall) Kitrinos KM. #1949 AASLD 2014. Manns M. EASL 2014

Baseline NS5A resistance and SOF/LDV Deep sequencing analysis of baseline samples (n=1904) in phase 2/3 SOF/LDV studies ELECTRON, LONESTAR and ION studies GT 1 (n=2137) No NS5A RAVs GT 1a (n=1602) NS5A RAVs GT 1b (n=529) Subjects with baseline NS5A RAVs are enriched in those who fail: 97% 16% of study population 96% 98% 93% 43% of those with virologic failure 92% 95% SVR12 (%) Sarrazin C. #1926 AASLD 2014.

Baseline NS5A resistance and SOF/LDV <100X >100X No RAVs Sarrazin C. #1926 AASLD 2014.

Impact of baseline NS5A RAVs on outcomes in retreatment No patients had SOF-associated variant, S282T, detected at baseline 2 patients had NS5B treatment-emergent variantl159f at baseline and achieved SVR 98% SVR 100% SVR 88% No NS5A RAVs at baseline n=44/50* 12% NS5A RAVs n=6/50 n=43/44 n=6/6 *1 patient s baseline results were not available. Wyles D. #235 AASLD 2014

Conclusions The next 18 months wont be as exciting Additional GT 1 regimens added: BMS Trio Grazoprevir/elbasvir SOF/GS-5816 GT2/3 We will have IFN-free regimens without RBV 12 weeks for GT3 Except cirrhosis? Data on 24 wks? 8 weeks with current investigational agents is about as short as we can go NS5A resistance likely impacts response Is the effect large enough to warrant baseline testing?

Thank You! My work is done.