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1 Corporate Presentation February 15, 2017 Creating Small Molecule Drugs for Viral Infections and Liver Diseases

2 Forward Looking Statements Disclaimer This presentation contains forward-looking statements concerning our business, operations and financial performance and condition, as well as our plans, objectives and expectations for our business prospects and the industry in which we operate. Any statements contained herein that are not statements of historical facts may be deemed to be forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as aim, anticipate, assume, believe, contemplate, continue, could, due, estimate, expect, goal, intend, may, objective, plan, predict, potential, positioned, seek, should, target, will, would, and other similar expressions that are predictions of or indicate future events and future trends, as well as other comparable terminology. All are forward-looking statements based on our management s current expectations, estimates, forecasts and projections about our business and the industry in which we operate and our management s beliefs and assumptions. These forward-looking statements are not guarantees of future performance or development and involve known and unknown risks, uncertainties and other factors that are in some cases beyond our control. These risks and uncertainties include the following: (i) our financial prospects for the next several years are dependent upon the development and commercializing efforts of AbbVie for combination therapies for HCV incorporating paritaprevir, or ABT-493, (ii) competition for these therapies, (iii) our prospects for successful development of any other HCV therapies, and (iv) the length, uncertainty and expense of discovering and developing new therapeutics for other diseases. As a result, any or all of our forward-looking statements in this presentation may turn out to be inaccurate. Please refer to these and other risk factors described or referred to in Risk Factors in Enanta s most recent Form 10-K, and other periodic reports filed with the Securities and Exchange Commission. Enanta cautions investors not to place undue reliance on the forward-looking statements contained in this presentation. These statements speak only as of the date of this presentation, and Enanta undertakes no obligation to update or revise these statements, except as may be required by law

3 Investment Highlights Virology & liver disease-focused biotech company Partnered Products: - Paritaprevir 1 st HCV protease inhibitor marketed in AbbVie regimens - Glecaprevir 2 nd HCV protease inhibitor NDA/MAA submitted by AbbVie for next-generation G/P combination FY2016 royalties on paritaprevir-containing regimens: $58 million Wholly-owned, clinical stage FXR agonist for NASH and PBC (EDP- 305, Ph1) R&D programs in HBV and RSV Strong balance sheet with approx. $244M cash at Dec. 31, 2016 Resources to fund clinical programs and to advance our R&D efforts

4 Expanding Beyond HCV Leverage our core strength in HCV to become a leader in Viral and Liver diseases Multiple therapeutic areas with goal of building multiple approaches in each HCV HBV NASH /PBC RSV

5 Broad Virology and Liver Disease Pipeline Product Candidate Discovery Preclin Phase 1 Phase 2 Phase 3 Launch HCV HCV NASH & PBC RSV HBV NASH NASH Protease Inhibitor Protease Inhibitor FXR Agonist EDP-305 Non-fusion Inhibitor Core Inhibitor FXR Agonist Follow-on Undisclosed paritaprevir - containing regimens glecaprevir - containing pan-genotypic 2-DAA combo EDP

6 HCV Market Market for HCV therapies: - Approx. $18B for 2016 Prevalence of chronic infection - US: ~ 2.7 to 3.9M (CDC) - Europe: ~ 15M* - Japan: ~ 1.5M to 2M** - Major genotype in U.S., E.U. and Japan is GT1 * EASL and HIV in Europe, The Number of People Living with Viral Hepatitis is Increasing, Press release Oct. 22, available from: ** Kohnodai Hospital. National Center for Global Health and Medicine [cited 20 February 2013]. Available from: Source:

7 Our HCV Opportunity Product Regimen Enanta Asset Economics 3-DAA (ABBV) paritaprevir (PI) Double-digit royalty on 30% of net sales 2-DAA (ABBV) paritaprevir (PI) Double-digit royalty on 45% of net sales (G/P) glecaprevir / pibrentasvir 2-DAA (ABBV) glecaprevir (PI) (ABT-493) Double-digit royalty on 50% of net sales

8 Glecaprevir (ABT-493) Pan-genotypic Protease Inhibitor (G/P) glecaprevir (PI) and pibrentasvir (NS5A) New 2-DAA regimen Breakthrough Therapy Designation granted U.S. NDA / EU MAA submitted - Priority Review / Accelerated Assessment - AbbVie targets approvals 2017 Once-daily, fixed-dose combination RBV-free Broad genotype profile (GT1-6) Excellent activity against key resistance mutants HCV Replicon Mean EC 50, nm GT 1a 0.85 ± 0.15 GT 1b 0.94 ± 0.35 GT 2a 2.7 ± 1.1 GT 3a 1.6 ± 0.49 GT 4a 2.8 ± 0.41 GT 6a 0.86 ± 0.11 Ng, et.al, CROI, Mar. 4, 2014 Ph3 data suggests a potential 8 week duration for the majority of patients

9 Glecaprevir (ABT-493): Phase 3 & Expanded Phase 2 Trials Enrollment >2,000 patients Phase 3 fixed-dose G/P combination of glecaprevir (300mg) + pibrentasvir (120mg) once daily Data readouts at AASLD Nov ( ) ENDURANCE-1 Non-cirrhotic GT1 SURVEYOR-2 Cirrhotic* GT3 ENDURANCE-2 Non-cirrhotic GT2 EXPEDITION-1 Cirrhotic* GT1,2,4-6 ENDURANCE-3 Non-cirrhotic GT3 EXPEDITION-2 HCV/HIV GT1-6 ENDURANCE-4 Non-cirrhotic GT4,5,6 EXPEDITION-4 Renal Impair. GT1-6 CERTAIN-1 GT1-6 (Japan) MAGELLAN-1 Prior DAA failures CERTAIN-2 GT2 (Japan) MAGELLAN-2 Liver/Kidney transplant *Child Pugh A cirrhotic patients

10 Glecaprevir / Pibrentasvir (G/P) Combo Preliminary Phase 3 Results: AASLD 2016 Study Name Non-Cirrhotic Patient Populations Treatment Duration SVR 12 Rate GT1 ENDURANCE-1 new to treatment, or not cured with previous IFN-based treatments* Includes patients co-infected w/ HIV-1 8 week 99% (n=348/ 351) ENDURANCE-3 new to treatment GT3 8 week 95% (n=149/ 157) SURVEYOR-2 (Part 4) GT2, 4, 5, or 6 new to treatment, or not cured with previous IFN-based treatments** 8 week 97% (n=196/ 203) * pegifn +/- RBV or SOF/RBV +/- pegifn ** pegifn, SOF/RBV or pegifn/sof Source: AbbVie/ Enanta press release: 11/11/

11 Virology & Liver Disease Focus Areas HCV NASH /PBC HBV RSV

12 Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH) Number one cause of liver disease in Western Countries NAFLD: excessive fat (triglyceride) accumulation in the liver (steatosis) A subgroup of NAFLD patients has liver cell injury and inflammation in addition to excessive fat (steatohepatitis), i.e. NASH NASH is associated with the metabolic syndrome diseases related to type 2 diabetes, insulin resistance, obesity, hyperlipidemia, and hypertension While NAFLD does not correlate with short-term morbidity or mortality, progression to NASH dramatically increases risks of cirrhosis, liver failure, and hepatocellular carcinoma Stages of Liver Injury (NIDDK)

13 Primary Biliary Cholangitis (PBC) Bile is a digestive liquid made in the liver that travels through bile ducts to the small intestine, where it helps in digestion PBC is a chronic inflammatory liver disease that slowly destroys bile ducts, causing bile to remain in the liver, leading to liver cell damage and cirrhosis As cirrhosis progresses and liver scar tissue increases, the liver loses its ability to function, leading to potential liver failure, liver transplantation, or hepatocellular carcinoma NIDDK

14 NASH and PBC Potential Markets NASH Currently no approved therapies US prevalence estimated to be 3%-5% (~9 to15 million) - 20% of whom likely to develop cirrhosis (Rinella, Hepatology, 2011) Patient pool size may rival HCV Prevalence of NASH likely to increase due to increase in underlying causes, e.g. obesity PBC Estimated US incidence: 4.5 cases for women and 0.7 cases for men per 100,000 population Two approved PBC therapies: - Ursodiol (ursodeoxycholic acid or UDCA); only effective in 50% of patients - OCALIVA, (OCA) in combination with UDCA in adults with an inadequate response to UDCA or as monotherapy in adults unable to tolerate UDCA Significant potential add-on value beyond NASH

15 Enanta s Approach to NASH and PBC Agonists of Farnesoid X Receptor (FXR) FXR is a nuclear receptor and main regulator of bile acid levels in liver and small intestine FXR responds to bile acids by regulating transcription of key enzymes and transporters Inflammation FXR agonists have ameliorated a number of the pathologies in NASH and PBC models, including an effect on fibrosis Clinical validation has been achieved in NASH and PBC with the FXR agonist 6- ECDCA (OCA) Bile Acid Regulation FXR Fibrosis Lipid Metabolism & Gluconeogenesis Source: Matsubara Mol Cell Endocrinol 2013; Neuschwander-Tetri et al, Lancet,

16 AhR AR CAR2 CAR3 ERα ER b FXR GR LXRα LXRb MR PGR PPARα PPARd PPARg PXR RARα RARb RARg RXRα RXRb RXRg TRα TRb VDR EDP-305 is a Potent and Selective FXR Agonist FXR activation (HEK cells) EDP-305 OCA* EC50 8 nm 130 nm Efficacy 152% 150% * OCA: Obeticholic acid EDP-305 Nuclear Receptor Selectivity relative activity, tested at 10uM TGR5 (bile acid receptor) CHO cells EDP-305 OCA EC50 >15,000 nm 380nM Efficacy NA 72% Source: Y. Li, et.al, AASLD

17 EDP-305 Suppresses Liver Injury and Fibrosis in a Murine Model of Steatohepatitis * 8-week male C57B16 mice Yury Popov, M.D., Ph.D. NASH-TAG 2017 Treatment with EDP-305 or OCA Vehicle (placebo) Harvard Medical School EDP and 30 mg/kg arms, QD x 4 weeks OCA 30 mg/kg QD x 4 weeks End-points: serum chemistry, hepatic collagen content and histology * MCD: methionine-choline deficient diet

18 Strong Inhibitory Effect on Liver Fibrosis Progression (biochemically via hydroxyproline) EDP-305 at 10 and 30 mg/kg had up to 70% reduction in hepatic collagen deposition (* p<0.05) No significant effect on collagen deposition by OCA in this model Yury Popov, M.D., Ph.D. NASH-TAG

19 Sinusoidal Fibrosis Suppressed in MCD Mice by EDP- 305 at 10 and 30 mg/kg Effect of treatments on fibrosis (via picrosirius red staining) Yury Popov, M.D., Ph.D. NASH-TAG

20 EDP-305 Reduces Fibrosis Progression by MR Imaging of BDL (bile duct ligation) Rats * EDP , 30 mg/kg QD OCA 10, 30 mg/kg QD Study compounds blinded to investigators Bryan C. Fuchs, Ph.D. AASLD 2016 A gadolinium-based collagen targeted probe was used for MR imaging of liver fibrosis

21 EDP-305 Treated Rats Have Less Fibrosis than BDL Only and OCA Groups Histological Analysis Biochemical Analysis BDL rats without drug Collagen Proportional Area Analysis of Sirius Red Staining Image J open source software Hydroxyproline EDP mg/kg OCA 10 mg/kg * P<0.05; ** P<0.01; ***P<0.001 OCA dosed at 10 mg/kg, toxicity at 30 mg/kg * P<0.05; ** P<0.01; ***P<0.001 Bryan C. Fuchs, Ph.D., AASLD

22 EDP-305 Decreases BDL Rat Fibrosis in Collagen-targeted Molecular MRI Fibrosis Imaging Relaxation Rate Analysis Sham BDL EDP mpk OCA 30 mpk P r e G d P o s t Bile duct Enlarged bile duct G d Intestine blue is food Liver orange is fibrosis Liver yellow: no or min fibrosis Imaged pre- and post-injection of collagen-targeted peptide probe More fibrosis with orange color * P < 0.05; ** P<0.01 Relaxation rate R1 measured prior to and 45 minutes post injection of probe DR1 was assessed as a measure of fibrosis Bryan C. Fuchs, Ph.D., AASLD

23 FXR Agonist EDP-305: Summary Potent FXR receptor agonist activity vs OCA Highly selective for FXR vs other nuclear receptors and vs TGR5 receptor Potent and differentiated effects on FXR-dependent gene expression vs OCA (e.g. Shp, Cyp7a1, Bsep, Fgf15) - human hepatocytes and in vivo mouse model Improvement in hepatocyte ballooning and overall NAFLD Activity Score vs OCA in STAM TM Mouse NASH model Reduced liver fibrosis in CDAHFD, MCD, and BDL rodent models Phase 1 study ongoing in healthy subjects and subjects with presumed NAFLD Fast Track Designation granted by FDA

24 Virology & Liver Disease Focus Areas HCV NASH /PBC HBV RSV

25 Respiratory Syncytial Virus (RSV) Negative-sense, single-stranded RNA virus of family Paramyxoviridae Most common cause of bronchiolitis (inflammation of the small airways in the lung) and pneumonia in children <1 year old in the U.S. Each year, 75,000 to 125,000 children in this age group are hospitalized due to RSV infection (most < 6 months old) Almost all children have had an RSV infection by age 2 When infants/children are exposed to RSV for first time, 25% to 40% have signs or symptoms of bronchiolitis or pneumonia Adults with compromised immune systems and those age 65+ are also at increased risk of severe disease No safe and effective treatments Source: CDC

26 First Clinical Candidate: EDP-938 for RSV Non-Fusion approach directly targets virus replication Nanomolar inhibitor of both RSV-A and RSV-B activity Maintained antiviral potency across all clinical isolates tested Demonstrated high-barrier to resistance in vitro Synergy with other drug mechanisms - e.g. fusion and L inhibitors Active against resistant virus from other mechanisms Robust in vivo efficacy data Goal: Initiate Ph1 in calendar 4Q

27 EDP-938 Dramatically Reduces Viral Load in BAL (Bronchoalveolar Lavage) Fluid Viral loads in EDP-938 treated animals were below the limit of detection (LOD) on days 3, 5 and 7 LOD 100 mg/kg BID of EDP-938 or vehicle control was given 24h prior to infection (day -1), on the day of infection (day 0), and for days

28 EDP-938 vs. ALS-8176: Efficacy at the End of Treatment (Day 5) in AGMs BAL** NP Swab*** LOD* 100 mg/kg BID of EDP-938 or vehicle control was given 24h prior to infection (day -1), on the day of infection (day 0), and for days 1-4 Loading dose of 200 mg/kg ALS-8176 given 24h prior to infection, followed by 50 mg/kg BID on the day of infection, and for 4 additional days.(deval et. al., PLoS Pathogens 2015) * LOD (limit of detection) ** BAL (bronchoalveolar lavage fluid) *** NP (nasopharyngeal) Swab

29 Virology & Liver Disease Focus Areas HCV NASH /PBC HBV RSV

30 Potentially life-threatening liver infection caused by the hepatitis B virus Current treatments rarely give true cures - Interferon gives better results (~10%), but with side effects - RT inhibitors very effective at reducing viral load, but offer very low cure rates (1% or lower) and must be taken for life to improve cirrhosis or HCC outcomes Prevalence estimates - US: ~550,000-2 million - US + Japan + major EU populations: ~4.9 million - Worldwide: ~240 million Estimated 15-25% of patients with chronic HBV infection will develop chronic liver diseases including cirrhosis, HCC, or liver decompensation Sources: WHO, CDC, Datamonitor HBV Background

31 HBV Program: Summary Current focus: Core Inhibitors - Clinical validation (Novira) - Exploring additional mechanisms with goal of a functional cure Pre-clinical lead optimization and IP activity ongoing Goal: Clinical candidate identification in

32 Financial Highlights ($ In millions) Fiscal Year Ended Sept. 30, 2016 Fiscal 1Q17 Total Revenues 88.3* $10.4 R&D Expenses $40.5 $12.5 G&A Expenses $17.0 $4.9 Net Income (loss) $21.7 $(5.0) EPS (per diluted share) $1.13 $(0.26) Balance Sheet Cash and Cash Equivalents $242.4 $244.4 * Includes $30M in payment earned from AbbVie for commercialization regulatory approval in Japan

33 Financial Summary Cash as of Dec. 31, 2016: Approx. $244M, no debt Double-digit royalties on allocated paritaprevir sales - FY2016 royalties: $58 million Financial opportunity from glecaprevir (ABT-493) - targeted approval 2017* - up to $80M in regulatory approval milestone payments - additional double-digit royalty opportunity on 50% of net sales * Source: AbbVie

34 Key Catalysts HCV HBV NASH /PBC RSV Glecaprevir (ABT-493): - U.S. NDA / EU MAA submitted; commercialization of G/P expected in 2017 (AbbVie) FXR agonist EDP-305 for NASH / PBC: - Ph1 data (healthy volunteers & presumptive NAFLD subjects) 2H Initiate Ph2 PBC trial and NASH-enabling studies 2H17 - Ph2 start in NASH in early Advance follow-on compounds RSV program: - Advance EDP-938 to Ph1 in 4Q17 HBV program: - Aiming for clinical candidate identification in

35 Creating Small Molecule Drugs for Viral Infections and Liver Diseases