8-K

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d)

of The Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): April 13, 2021

Akero Therapeutics, Inc.

(Exact name of registrant as specified in its charter)

Delaware	001-38944	81-5266573
(State or other jurisdiction of incorporation)	(Commission File Number)	(I.R.S. Employer Identification No.)

601 Gateway Boulevard, Suite 350 South San Francisco, CA	94080
(Address of principal executive offices)	(Zip Code)

Registrant’s telephone number, including area code (650) 487-6488

Not Applicable

(Former name or former address, if changed since last report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

¨ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

¨ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

¨ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

¨ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class	Trading symbol(s)	Name of each exchange on which registered
Common Stock, par value $0.0001 per share	AKRO	The Nasdaq Global Select Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).

Emerging growth company x

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ¨

Item 8.01. Other Events.

The Company from time to time presents and/or distributes to the investment community at various industry and other conferences slide presentations to provide updates and summaries of its business. A copy of its current corporate slide presentation is being filed herewith as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated herein by reference. The Company undertakes no obligation to update, supplement or amend the materials attached hereto as Exhibit 99.1.

Item 9.01. Financial Statements and Exhibits.

(d) Exhibits

Exhibit No.	Description
99.1	Corporate slide presentation of Akero Therapeutics, Inc.

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

Date: April 13, 2021	AKERO THERAPEUTICS, INC.
	By:	/s/ Andrew Cheng
		Andrew Cheng, M.D., Ph.D. President and Chief Executive Officer

EX-99.1

Exhibit 99.1

A Global Disease, A Pioneering Treatment Corporate Presentation April 2021

- CONFIDENTIAL - CORPORATE HIGHLIGHTS 2 • Human FGF21 analog addresses all core aspects of NASH pathology • Engineered for optimal activity and convenient once - weekly dosing • We believe Phase 2a BALANCED study results among strongest data in field for both F1 - F3 and cirrhotic (F4) patients • Generally well - tolerated • EFX designated as a Priority Medicine (PRIME) based on strength of Phase 2a data • Plan to pursue marketing approval in 2 distinct patient populations: F2/F3 & F4 NASH • Dosed first patient in Ph2b HARMONY study in F2/F3 patients with 28 and 50mg doses in March • Expect to initiate Ph2b SYMMETRY study in cirrhotic (F4) patients in 2H’21 • Expect to manufacture Phase 3 API in 2H’21 • Involved in 20+ FDA approvals • Extensive experience in drug discovery, development and commercialization Efruxifermin (EFX): Potential Leading NASH Monotherapy Regulatory Status 2021 Milestones (Completed & Upcoming) Experienced Team

- CONFIDENTIAL - 3 EXTENSIVE DEVELOPMENT AND COMMERCIALIZATION EXPERIENCE INVOLVED IN 20+ MEDICINE APPROVALS Andrew Cheng, MD, PhD | President & CEO • 19 years at Gilead • Chief Medical Officer & HIV Division Head • Major role in 11 NDA/MAA approvals Kitty Yale | EVP & Chief Development Officer • Over 25 years at Gilead, Roche, Pfizer • VP, Gilead Worldwide Clinical Operations • Major role in 8 global approvals NDA, MAA, JNDA and CFDA William White | EVP, CFO & Head of Corporate Development • 18 years in life sciences investment banking at Goldman Sachs, Citigroup and Deutsche Bank • Most recently, Head of US Life Sciences Investment Banking at Deutsche Bank • Advised on more than $70bn in M&A and $25bn in financing transactions Jonathan Young, PhD, JD | Founder, EVP & COO • Over 15 years in biotechnology product development, law and regulatory policy • General Counsel and VP Policy, Braeburn • Partner and General Counsel, FoxKiser Tim Rolph , D.Phil | Founder & CSO • Over 30 years at Pfizer & Glaxo • CSO of Pfizer’s cardiovascular and metabolic disease unit • Head of Groton & UK Discovery Research, Pfizer • Major role in discovery and early clinical evaluation of two medicines: Selzentry (HIV) and Steglatro (Diabetes)

- CONFIDENTIAL - NASH: A SERIOUS AND DEBILITATING MULTI - SYSTEM DISEASE 4 An estimated 17 million Americans have NASH, with expectation that population will grow >50% by 2030 The number of NASH patients with advanced - stage fibrosis and cirrhosis is predicted to grow to 8 million in the US by 2030, an increase of approximately 140% from 2015 NASH is a leading cause of liver transplantation in the US and Europe NASH epidemic fueled by rise in obesity and diabetes No treatments currently available The leading cause of death for NASH patients is cardiovascular disease

- CONFIDENTIAL - 5 CIRRHOTIC NASH PATIENTS HAVE POOR PROGNOSIS ~60% 5 - year mortality for F4 NASH patients absent transplant 0 5 10 15 20 25 30 F0 F1 F2 F3 F4 Liver - related mortality rate increases substantially from F3 to F4 fibrosis Liver - Related Mortality 0 0 Fibrosis Stage Rate (per 1,000 PYF) Survival Free of Liver Transplantation Follow - up (years) Cumulative Survival (%) Angulo, P et al. (2015) Gastroenterology 149:389 - 397 Fibrosis Stage Dulai , PS et al. (2017) Hepatology 65:1557 - 65

- CONFIDENTIAL - EFX ENGINEERING POTENTIALLY OPTIMAL FOR NASH EFFICACY, WITH CONVENIENT ONCE - WEEKLY DOSING 6 Key attributes Stanislaus, S et al. (2017) Endocrinology 158(5): 1314 - 27; Lee, S et al. (2018) Nature 553: 501 - 505; Kharitonenkov, A et al. (2007) Endocrinology 148(2)774 - 781 Akero proprietary Fc - FGF21, Point mutations Increases half - life from < 2 hours to 3 - 4 days High affinity for β - Klotho Balanced potency at FGFR1c, 2c, 3c Better translation to human pharmacology Inactive at FGFR4

- CONFIDENTIAL - EFX ACTS ON TWO MAJOR SOURCES OF LIVER FAT WITH POTENTIAL FOR OPTIMAL REDUCTION 7 Source of Liver Fat FGF Receptor EFX Activity Lipolysis FGFR1c x De Novo Lipogenesis FGFR2c FGFR3c x Sources of Fat Flowing into and Through Liver for NASH Patients Adipose Tissue: Lipolysis (40 - 50%) FGFR1c Liver: De Novo Lipogenesis (30 - 40%) FGFR2c, 3c Dietary Fat (10 - 20%) Lambert, JE et al. (2014) Gastroenterology 146(3): 726 - 35 Acting on both hepatic and peripheral sources of liver fat is key to optimizing liver fat reduction

- CONFIDENTIAL - EFX DIRECT AND INDIRECT ANTI - FIBROTIC EFFECTS 8 Myofibrobl asts *Cited literature available on company website Bao, L et al. (2018) Br J Pharmacol 175:3379 - 3393; Fisher, FM et al. (2014) Gastroenterology 147:1073 - 1083.e6; Jimenez, V et al. (2018) EMBO Mol Med 10:e8791; Lee, JH et al. (2016) Am J Transl Res 8:4750 - 4763; Sanyal, A et al. (2018) Lancet 392:2705 - 2717; Le, CT et al. (2018) PLOS one 13:e0192146; Xu, P et al. (2016) Toxicol Appl Pharmacol 290:43 - 53; Yu, Y et al. (2016) Int Immunopharmacol 38:144 - 152 EFX Hepatocyte Stress & Death Myofibroblast Differentiation Kupffer Cell Activation Fibrosis Direct Effect Indirect Effect

- CONFIDENTIAL - Screening Biopsy - Confirmed NASH Randomization 70mg EFX (n=20) 50mg EFX (n=20) 28mg EFX (n=20) Placebo (n=20) Safety Follow - Up Responder Paired Biopsies Week 6 Week 12 Screening Post - Treatment 16 WEEKS Subjects achieving ≥30% relative reduction of hepatic fat at week 12 eligible for post - treatment biopsy; biopsy scoring based on NASH CRN 9 PHASE 2A TRIAL (BALANCED) DESIGN (F1 - F3 NASH) Key Secondary Endpoints • Relative Liver Fat • Response Rate • ALT MRI - PDFF Liver Biopsy Key Exploratory Efficacy Endpoints • 2 - Point NAS Improvement • Fibrosis Improvement • NASH Resolution • Serum Pro - C3 Primary Endpoint • Absolute Liver Fat

- CONFIDENTIAL - * PHASE 2A EXPANSION COHORT C TRIAL DESIGN (F4 NASH) 10 Primary Endpoint Safety & tolerability BALANCED study included an expansion cohort, Cohort C, of patients with compensated cirrhosis (F4), Child - Pugh Class A; results to inform subsequent development in cirrhotic patients 16 Weeks Screening Randomization EFX 50 mg (n=20) Placebo (n=10) FibroScan Liver Biopsy Fibrosis Biomarkers (ELF, Pro - C3) * Protocol amended to include voluntary end - of - treatment biopsies

- CONFIDENTIAL - BASELINE DEMOGRAPHICS: MAIN STUDY & COHORT C BALANCED Main a Cohort C b Parameter Mean Placebo (N=21) EFX 28mg (N=19) EFX 50mg (N=20) EFX 70mg (N=20) Placebo (N=10) EFX 50mg (N=20) Age (Years) 52 50 53 53 57.1 61.1 Sex (Male/Female) 6/15 9/10 10/10 9/11 7/3 4/16 Weight (kg) 99.6 108.2 103.6 103.1 119.1 97.9 NAFLD Activity Score (NAS) (range) 5.1 (4 to 7) 5.6 (4 to 7) 5.1 (3 to 7) 5.6 (5 to 7) 3.4 c (1 to 6) 4.2 c (1 to 7) Alanine Aminotransferase (ALT) ( U/L) 50.7 62.5 53.4 56.8 32.7 31.7 Aspartate Aminotransferase (AST) (U/L) 38.6 41.1 35.4 44.6 28.9 31.4 % Type 2 Diabetes 67 37 50 50 50 50 HbA1c (%) 6.5 6.2 6.4 6.2 6.5 6.1 Triglycerides (mg/dL) 208 176 177 180 122 135 ELF Score 9.4 9.5 9.5 9.6 9.7 10.4 Pro - C3 ( μ g/L) 16.1 19.2 16.2 17.2 22.6 25.6 Liver Stiffness ( kPA ) 11.9 12.5 11.3 12.4 25.8 22.1 11 a Full Analysis Set, F1 - F3 (all subjects randomized into the BALANCED main study); b Full Analysis Set, F4 (all subjects randomized into BALANCED Cohort C [except where otherwise noted]); c Liver Biopsy Analysis Set, F4 (all Cohort C subjects confirmed by central reader as F4 at baseline with Week 16 liver biopsy re sults)

- CONFIDENTIAL - HIGH RATES OF FIBROSIS IMPROVEMENT AFTER 16 WEEKS ACROSS ALL DOSE GROUPS (F1 - F3 NASH) 12 Source Data: Liver Biopsy Evaluable Analysis Set, F1 - F3 (all BALANCED main study responders who had baseline and end - of - treatmen t liver biopsy results) 0% 10% 20% 30% 40% 50% 60% 70% Overall 0% 10% 20% 30% 40% 50% 60% 70% Overall Fibrosis Improvement ≥1 Stage and No Worsening of NASH 1,2 1 Improvement in liver fibrosis greater than or equal to one stage and no worsening of NASH (defined as no increase in NAS for ballooning, inflammation, or steatosis) 2 Secondary and exploratory histological endpoints were not powered for statistical significance Placebo N=2 0% All EFX N=40 48% 19 28 mg N=13 46% 6 50 mg N=13 62% 8 70mg N=14 36% 5 Biopsy Reading • All baseline and end - of - treatment biopsies were centrally read by a single NASH - CRN pathologist • Baseline biopsies were not re - read with end - of - treatment biopsies • All biopsies were read blinded to both treatment assignment and patient

- CONFIDENTIAL - 9% 23% 68% Improved No Change Worsened 9% 23% 68% 2 13 FIBROSIS IMPROVEMENT IN F2 - F3 PATIENTS: HALF OF PATIENTS IMPROVED 2 STAGES All EFX Patients (n=40) Baseline F2 - F3 EFX Patients (n=22) 2 - Stage Improvement (n=11, 50%) 1 - Stage Improvement (n=4, 18%) 10% 35% 55% Source Data: Liver Biopsy Evaluable Analysis Set, F1 - F3 Change in liver fibrosis

- CONFIDENTIAL - HIGH RATE OF FIBROSIS IMPROVEMENT AFTER ONLY 16 WEEKS AMONG CIRRHOTIC PATIENTS (F4 NASH) 14 Source Data: Liver Biopsy Analysis Set, F4; Topline preliminary data 1 No increase in NAS for ballooning, inflammation, or steatosis 2 Study not powered to assess statistical significance of changes in histological endpoints 0% 10% 20% 30% 40% Overall Fibrosis Improvement ≥1 Stage Without Worsening of NASH 1,2 Placebo n =5 0% EFX 50mg n =12 33% 4 Biopsy Reading • All baseline and end - of - treatment biopsies were read by a single NASH - CRN pathologist • All biopsies were read blinded to both treatment assignment and patient • Baseline biopsies were read independently of end - of - treatment biopsies, in random fashion and not paired Baseline Biopsy Timing • Mean time from historical biopsy to patient screening = 6 months

- CONFIDENTIAL - -50% -40% -30% -20% -10% 0% 10% BL W1 W4 W8 W12 Placebo 28mg 50mg 70mg *** *** *** Pro - C3, LS Mea n Change from Baseline RAPID IMPROVEMENTS IN FIBROSIS BIOMARKERS CONSISTENT WITH HISTOLOGICAL IMPROVEMENTS (F1 - F3 NASH) 15 Enhanced Liver Fibrosis (ELF) Score, LS Mean *** p<0.001, versus placebo (MMRM) Dose Group Baseline Δ Week 12 Placebo 9.4 0.0 28mg 9.5 - 0.7 *** 50mg 9.5 - 0.8 *** 70mg 9.6 - 0.4 * * p<0.05, *** p<0.001 versus placebo (ANCOVA) Pro - C3, LS Mean (ug/L) Dose Group Baseline Δ Week 12 Placebo 16.1 - 1.5 28mg 19.2 - 6.1 *** 50mg 16.2 - 5.9 *** 70mg 17.2 - 6.7 *** Source Data: Full Analysis Set, F1 - F3 *** *** *** *** *** ***

- CONFIDENTIAL - IMPROVEMENTS IN FIBROSIS BIOMARKERS IN CIRRHOTIC NASH PATIENTS SUPPORT HISTOLOGY RESULTS (F4 NASH) Source Data: Biomarker Analysis Set, F4 (all Cohort C subjects with baseline and interpretable on - study measure of ELF or pro - C3 , respectively); Liver Stiffness Analysis Set, F4 (all Cohort C subjects with baseline and interpretable on - study measure of Liver Stiffness); Topline preliminary data LS Mean Change From Baseline to Week 16 -0.4 -0.3 -0.2 -0.1 0.0 0.1 0.2 0.3 CFB ELF Score ** p<0.01, versus placebo (ANCOVA) - 0.4 ** +0.3 -10 -8 -6 -4 -2 0 CFB - 9.0 * - 3.4 Pro - C3 (µg/L) * p<0.05, versus placebo (ANCOVA) -6 -5 -4 -3 -2 -1 0 CFB - 5.7 †† - 1.9 Liver Stiffness 1 (kPa) †† p<0.01, versus baseline (ANCOVA) 1 Measured by FibroScan EFX 50mg Placebo EFX 50mg Placebo EFX 50mg Placebo 16 n =20 n=10 n =20 n=10 n =20 n=10

- CONFIDENTIAL - 17 INTERPRETING THE RAPID REVERSAL OF FIBROSIS OBSERVED IN NASH PATIENTS TREATED WITH EFX Indirectly anti - fibrotic Directly anti - fibrotic ↓ Hepatocyte Stress ↓ Inflammation ↓ Liver fat ↓ Collagen Synthesis EFX • Addressing underlying NASH disease drivers may indirectly contribute to fibrosis reversal for F1 - F3 patients with adequate time for the liver to regenerate • Redress of the underlying NASH disease drivers is necessary to sustain fibrosis reversal in F1 - F4 • Supports broader metabolic improvements • Fibrosis reversal in cirrhotic patients (F4), two - stage improvement of fibrosis in F2/F3 patients, and corroborating non - invasive markers of fibrosis improvement likely reflects direct anti - fibrotic activity • Fibrosis reversal is especially advantageous for cirrhotic patients who face high risk of mortality and severe morbidity

- CONFIDENTIAL - SUBSTANTIAL REDUCTIONS IN LIVER FAT AT WEEK 12 ACROSS ALL DOSE GROUPS (F1 - F3 NASH) 18 Source Data: Full Analysis Set, F1 - F3 -15 -12 -9 -6 -3 0 Placebo 28mg 50mg 70mg - 0% - 12.3 *** - 13.4 *** - 14.1 *** Absolute Reduction (%) *** p<0.001, versus placebo (ANCOVA) LS Mean Reduction in Liver Fat Baseline 22.2% Liver Fat Week 12 2.0% Liver Fat (↓90%) Analyzed with Liver MultiScan MRI - PDFF Images for Patient Treated with 50mg EFX Proton Density Fat Fraction (PDFF) Placebo 28mg 50mg 70mg - 72% - 63 % - 71%

- CONFIDENTIAL - -60% -40% -20% 0% 20% 40% BL W1 W4 W8 W12 W16 W20 Placebo 28 mg 50 mg 70 mg *** *** *** *** *** *** -60% -40% -20% 0% 20% 40% BL W1 W4 W8 W12 W16 W20 Placebo 28mg 50mg 70mg *** *** *** *** ** ** *** *** *** ALT, LS Mean Change from Baseline SUBSTANTIAL REDUCTIONS IN MARKERS OF LIVER INJURY AFTER 16 WEEKS OF TREATMENT (F1 - F3 NASH ) 19 AST, LS Mean Change from Baseline ** p<0.01, *** p<0.001, versus placebo (MMRM) *** *** *** Source Data: Full Analysis Set, F1 - F3 *** *** *** *** *** *** Similar dose - related improvements observed for GGT & ALP *** p<0.001, versus placebo (MMRM)

- CONFIDENTIAL - HIGH RESPONSE RATES ON NASH RESOLUTION AFTER 16 WEEKS ACROSS ALL DOSE GROUPS (F1 - F3 NASH) 20 Source Data: Liver Biopsy Evaluable Analysis Set, F1 - F3 1 NAS score of 0 or 1 for lobular inflammation and a score of 0 for ballooning 2 Secondary and exploratory histological endpoints were not powered for statistical significance * A single placebo responder lost 25 pounds over 16 weeks (11% weight reduction) 0% 10% 20% 30% 40% 50% 60% 70% Overall 0% 10% 20% 30% 40% 50% 60% 70% Overall NASH Resolution 1,2 and No Worsening of Fibrosis Placebo N=2 50% 1 * All EFX N=40 48% 19 28 mg N=13 46% 6 5 0mg N=13 54% 7 70mg N=14 43% 6

- CONFIDENTIAL - NASH RESOLUTION ALSO OBSERVED IN CIRRHOTIC PATIENTS (F4 NASH) 21 0% 10% 20% 30% Overall 1 NAS score of 0 or 1 for lobular inflammation and a score of 0 for ballooning 2 Study not powered to assess statistical significance of histological endpoints NASH Resolution 1,2 Placebo n=5 0% EFX 50mg n=12 25% 3 Source Data: Liver Biopsy Analysis Set; Topline preliminary data Change in NAS among Subjects Achieving NASH Resolution EFX Subject Baseline NAS Week 16 NAS A 7 1 B 3 1 C 6 1 Proportion of Subjects with ≥2 Point NAS Reduction Placebo EFX 50mg 1 (20%) 7 (58%)

- CONFIDENTIAL - DRUG - RELATED TREATMENT - EMERGENT ADVERSE EVENTS (TEAE) (F1 - F3 NASH) Most Common (>10%) Drug - Related AEs * Placebo (N=21) All EFX (N=58) EFX 28mg (N=19) EFX 50mg (N=19) EFX 70mg (N=20) Diarrhea 2 (10%) 21 (36%) 5 (26%) 10 (53%) 6 (30%) Nausea 0 (0%) 20 (34%) 6 (32%) 4 (21%) 9 (45%) Increased appetite 1 (5%) 13 (22%) 4 (21%) 4 (21%) 5 (25%) Vomiting 0 (0%) 9 (16%) 5 (26%) 2 (11%) 2 (10%) Frequent bowel movements 0 (0%) 8 (14%) 3 (16%) 2 (11%) 3 (15%) Abdominal pain 0 (0%) 7 (12%) 1 (5%) 3 (16%) 3 (15%) Injection site erythema 0 (0%) 7 (12%) 2 (11%) 0 (0%) 5 (25%) Injection site reaction 0 (0%) 6 (10%) 2 (11%) 1 (5%) 3 (15%) Fatigue 2 (10%) 6 (10%) 0 (0%) 1 (5%) 5 (25%) TEAE/SAE Disposition Placebo All EFX 28mg 50mg 70mg TEAE Leading to Death 0 0 0 0 0 TEAE Leading to Discontinuation 1 a 6 2 b 0 4 c Serious Adverse Event (SAE) 0 2 1 d 0 1 22 *Across EFX dose groups Source Data: Safety Set, F1 - F3 (all BALANCED main study subjects who received at least one dose of study drug a Muscular Weakness & Myalgia; b Nausea, Vomiting & Dysgeusia; Panic Attack and Anxiety - Linked Tremor; c Dysphagia (Not Drug Related); Acute Pancreatitis (also an SAE); Vomiting; Fatigue & Nausea; d Related to pre - dosing liver biopsy

- CONFIDENTIAL - Key Observations • Encouraging tolerability given population with more advanced disease • All injection site AEs Grade 1 • No reports of tremor TOLERABILITY OVERVIEW (F4 NASH) Most Frequent (>15%) Drug - Related AEs Placebo (N=10) EFX 50mg (N=17) Diarrhea 1 (10%) 7 (41%) Nausea 1 (10%) 5 (29%) Injection site reaction 0 5 (29%) Injection site erythema 0 4 (24%) Headache 0 3 (18%) TEAE/SAE Disposition Placebo EFX 50mg Study Discontinuations 1 a 1 b Serious Adverse Events (SAE) 1 c 0 Deaths 0 0 23 a Withdrawal of consent b abdominal distension, constipation, diarrhea, pruritus c pulmonary embolism Source Data: Safety Set, F4 (all Cohort C subjects confirmed by central reader as F4 at baseline who received at least one dose of study drug); Topline preliminary data

- CONFIDENTIAL - -4 -3 -2 -1 0 W16 70mg -4 -3 -2 -1 0 BL W1 W4 W8 W12 W16 Placebo 28mg 50mg 70mg Mean Change in Body Weight (kg) 24 WEIGHT LOSS OBSERVED FOR ALL DOSE GROUPS (F1 - F3 NASH) Mean Change in Body Weight at Week 16 (kg) Source Data: Full Analysis Set, F1 - F3 Placebo 28mg 50mg - 0.3 - 2.3 - 3.7 + 0.1

- CONFIDENTIAL - -20% -15% -10% -5% 0% W16 - 16% - 2% - 6% 0% * Placebo 28mg 50mg 70mg -25% -20% -15% -10% -5% 0% W16 - 22% - 15% - 17% - 1% *** * ** Placebo 28mg 50mg 70mg 0% 10% 20% 30% 40% 50% W16 + 34% + 39% + 41% + 4% *** *** *** Placebo 28mg 50mg 70mg IMPROVED LIPOPROTEIN PROFILE (F1 - F3 NASH) 25 LDL Cholesterol HDL Cholesterol Non - HDL Cholesterol LS Mean Change From Baseline to Week 16 (%) * p<0.05, ** p<0.01, *** p<0.001, versus placebo (ANCOVA) -50% -40% -30% -20% -10% 0% 10% W16 - 39% - 48% - 46% + 6% *** *** *** Placebo 28mg 50mg 70mg Triglycerides Source Data: Full Analysis Set, F1 - F3 * p<0.05, versus placebo (ANCOVA) *** p<0.001, versus placebo (ANCOVA) *** p<0.001, versus placebo (ANCOVA)

- CONFIDENTIAL - -0.9 -0.8 -0.7 -0.6 -0.5 -0.4 -0.3 -0.2 -0.1 0.0 0.1 W16 CLINICALLY MEANINGFUL IMPROVEMENTS IN GLYCEMIC CONTROL AFTER 16 WEEKS (F1 - F3 NASH) 26 LS Mean Change From Baseline to Week 16 (%) 1 Absolute change from baseline, % Type 2 DM Patients (N=41) + 0.1 - 0.6 - 0.9 + 0.0 Placebo 28mg 50mg 70mg ** -0.9 -0.8 -0.7 -0.6 -0.5 -0.4 -0.3 -0.2 -0.1 0.0 0.1 W16 All Patients (N=80) Placebo 28mg 50mg 70mg * ** - 0.1 - 0.4 - 0.5 +0.1 HbA1c 1 * p<0.05, ** p<0.01, versus placebo (ANCOVA) -30% -20% -10% 0% 10% 20% W16 - 27% - 28% - 33% - 5% * Placebo 28mg 50mg 70mg * -30% -20% -10% 0% 10% 20% W16 * Placebo 28mg 50mg 70mg Type 2 DM Patients (N=41) C - Peptide 2 All Patients (N=80) 2 Relative percent change from baseline - 24% - 22% - 29% + 21% Source Data: Full Analysis Set, F1 - F3 * * * p<0.05, versus placebo (ANCOVA)

- CONFIDENTIAL - NASH DEVELOPMENT LANDSCAPE: FIBROSIS IMPROVEMENT (F1 - F3) 27 Proportion of Subjects with ≥1 Stage Improvement in Fibrosis and No Worsening of NAS 1 1 FDA Guidance for Industry: Noncirrhotic Nonalcoholic Steatohepatitis With Liver Fibrosis: Developing Drugs for Treatment (201 8) Pbo All Pbo 1mg Pbo 0.8g 1.2g Pbo 10mg 25mg Pbo 0.2mg 0.4mg Pbo 20mg 50mg Intercept Ocaliva 78 Wks (Ph3) Daily Oral NGM Bio Aldafermin 24 Wks (Ph2a) Daily Injection (N=22) (N=50) Madrigal Resmetirom 36 Wks (Ph2a) Daily Oral (N=34) (N=79) (N=311) (N=308) Novo Nordisk Semaglutide 72 Wks (Ph2b) Daily Injection Cymabay Seladelpar 52 Wks (Ph2a) Daily Oral (N=25) (N=46) Inventiva Lanifibranor 24 Wks (Ph2b) Daily Oral (N=62) (N=69) Akero Efruxifermin 16 Wks (Ph2a) Weekly Injection (N=80) (N=82) (N=312) (N=78) (N=42) (N=63) 18 % 38 % 29 % 24 % 12 % 18 % 23 % 34 % 36% 48 % 20 % 24% 37 % 32% 46 % 29% Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. No head - to - head clinical trials have been conducted. Inventiva (2020) June 16 Corporate Presentation; NGM Bio (2020) June 3 Corporate Presentation; Harrison, S et al. (2019) Lancet 394(10213):2012 - 24; CymaBay (2020) March 12 Press Release; Novo Nordisk (2020) June 19 R&D Investor Presentation; Younossi Z et al. (2019) Lancet 394(10215):2184 - 96. All trademarks are the property of their respective owners. Increasing dosing duration 78 Wks Pbo All EFX 50mg (N=2) (N=13) (N=40) 0 % 62% 48% 24 Wks

- CONFIDENTIAL - Belapectin 52 Wks (Ph2b) Oral GAL - 3 COHORT C RESULTS IN CONTEXT: FIBROSIS IMPROVEMENT * (F4) Selonsertib 48 Wks (Ph3) Oral Simtuzumab 96 Wks (Ph2b) IV infusion ASK - 1 ACC FXR LOXL2 Firsocostat 48 Wks (Ph2b) Oral Cilofexor 48 Wks (Ph2b) Oral (n=20) (n=21) Pbo 20mg Efruxifermin 16 Wks (Ph2a) SC Injection Fc - FGF21 (n=19) (n=21) Pbo 30mg (n=12) (n=5) Pbo EFX 50mg (n=46) (n=45) Pbo 2mpk (n=41) 8mpk (n=75) (n=75) Pbo 200mg (n=79) 700mg (n=351) (n=172) Pbo 6mg (n=354) 18mg 13 14 13 8 13 8 2 5 7 14 16 14 15 0 33 28 Increasing dosing duration 96 Wks 48 Wks Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. No head - to - head clinical trials have been conducted. * Results from all publicly reported NASH studies for single agents in F4 patients reporting either ≥ 1 - stage fibrosis improvement ( belapectin and simtuzumab ) or ≥ 1 - stage fibrosis improvement and no worsening of NASH (EFX, selonsertib , firsocostat and cilofexor ); numerical values represent percent responders Harrison, SH et al. (2020) J Hepatol 73(1):26 - 39; Loomba, R et al. (2020) Hepatol 73(2):625 - 43; Chalasani, N et al. (2020), Gastro 158:1334 – 45; Harrison, SH et al. (2018) Gastro 155:1140 - 53

- CONFIDENTIAL - Pbo 0.8g 1.2g Increasing dosing duration NASH DEVELOPMENT LANDSCAPE: NASH RESOLUTION (F1 - F3) 29 Proportion of Subjects with Resolution of NASH and No Worsening of Fibrosis 1 1 FDA Guidance for Industry: Noncirrhotic Nonalcoholic Steatohepatitis With Liver Fibrosis: Developing Drugs for Treatment (201 8) Pbo 20mg 50mg Pbo 10mg 25mg Pbo 0.2mg 0.4mg Pbo All Pbo 1mg Intercept Ocaliva 78 Wks (Ph3) Daily Oral NGM Bio Aldafermin 24 Wks (Ph2a) Daily Injection (N=22) (N=50) Madrigal Resmetirom 36 Wks (Ph2a) Daily Oral (N=34) (N=79) (N=311) (N=308) Novo Nordisk Semaglutide 72 Wks (Ph2b) Daily Injection Cymabay Seladelpar 52 Wks (Ph2a) Daily Oral (N=25) (N=46) Inventiva Lanifibranor 24 Wks (Ph2b) Daily Oral (N=62) (N=69) Akero Efruxifermin 16 Wks (Ph2a) Weekly Injection (N=80) (N=82) 9 % 24 % 25 % 15 % 8 % 26 % 23 % 23 % 67 % 8 % 12 % (N=312) (N=78) (N=42) 19% 11% (N=63) 40 % 47% 78 Wks * A single placebo responder lost 25 pounds over 16 weeks (11% weight reduction) Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. No head - to - head clinical trials have been conducted. Inventiva (2020) June 16 Corporate Presentation; NGM Bio (2020) June 3 Corporate Presentation; Harrison, S et al. (2019) Lancet 394(10213):2012 - 24; CymaBay (2020) March 12 Press Release; Novo Nordisk (2020) June 19 R&D Investor Presentation; Younossi Z et al. (2019) Lancet 394(10215):2184 - 96. All trademarks are the property of their respective owners. Pbo All EFX 50mg (N=2) (N=13) 48% 54 % (N=40) * 50 % * 49 % 24 Wks

- CONFIDENTIAL - NEXT STEPS FOR EFX: PARALLEL 2B TRIALS IN F2/F3 & F4 BALANCED Cohort C (Expansion of BALANCED) HARMONY SYMMETRY Status Completed (Readout Jun’20) Completed (Readout Mar’21) Ongoing (Initiated Feb’21) Expected to be initiated 2H’21 Duration 16 Weeks 16 Weeks 24 Weeks Under review EFX Arms 28, 50, 70mg 50mg 28, 50mg Under review Placebo - Controlled x x x x F1 - F3 F4 F2/F3 F4 Phase 2a Phase 2b 30 Biopsy - Confirmed:

- CONFIDENTIAL - PHASE 2B (F2/F3) TRIAL DESIGN (HARMONY) Screening Randomization EFX 28mg Placebo 24 Weeks EFX 50 mg Placebo EFX * Long - Term Safety Follow - Up Phase 2b MRI - PDFF Liver Biopsy * Phase 3 protocol finalization expected after end - of - Phase 2 meeting with FDA Key Inclusion Criteria • F2 - 3 NASH • NAS ≥4 • Liver fat ≥8% Phase 2b Primary Endpoint • Fibrosis Improvement K ey Secondary Efficacy Endpoints • NASH Resolution • Fibrosis Markers • Lipoproteins • Glycemic Control • Weight Change • MRI - PDFF • Liver Injury Markers EOP2 Meeting Phase 3 Initiation *

- CONFIDENTIAL - 32 STRONG FINANCIAL POSITION ~$ 106M Raised in aggregate gross proceeds ~$ 268M COMPLETED UPSIZED FOLLOW - ON OFFERING July 10, 2020 ~$ 216M Raised in aggregate gross proceeds

- CONFIDENTIAL - March June BALANCED F1 - F3 MRI - PDFF Read - out June ~$106M Upsized IPO July BALANCED Initiation BALANCED F1 - F3 Liver Biopsy Read - out 2019 2020 CONSISTENT RECORD OF MILESTONE DELIVERY 33 July ~$216M Upsized Offering March BALANCED F4 Liver Biopsy Read - out February HARMONY F2/F3 Ph2b Initiation 2021 June $45.5M Series B Amgen License $45M Series A December 2018 2H (Expected) SYMMETRY F4 Ph2b Initiation 2H (Expected) HARMONY F2/F3 Ph2b Read - out 2022

Backup Slides

- CONFIDENTIAL - 35 PATIENT DISPOSITION (BALANCED MAIN STUDY) Randomized (80) MRI - PDFF Responders (50) (≥ 30% Relative Reduction) Week 12 MRI - PDFF (68) End - of - Treatment Biopsies Collected (42) Randomized Not Dosed EFX (1) Discontinued (11) Non - Responders Placebo (18) Dosed (79) Due to AEs EFX (6) - Pbo (1) Administrative EFX (4) Biopsies Not Collected Due to COVID - 19 EFX (8) 28mg (13) 50mg (13) 70mg (14) Placebo (2)

- CONFIDENTIAL - 36 PATIENT DISPOSITION (BALANCED COHORT C) Randomized/Dosed (n=30) End - of - Treatment Biopsies Collected (n=17 ) Confirmed F4 (n=27 ) Due to AEs EFX(1) Discontinued (2) Withdrawn Consent Placebo (1) EFX 50mg (12) Placebo (5) Not Confirmed F4 by central reader (3) Did not consent to end - of - treatment biopsy (8)

- CONFIDENTIAL - MAGNITUDE OF LIVER FAT REDUCTION (F1 - F3 NASH ) 37 Source Data: MRI - PDFF Evaluable Analysis Set (all BALANCED main study subjects who had baseline and Week 12 MRI - PDFF Proportion of Patients Achieving Fat Reduction Thresholds at Week 12 Endpoint Placebo 1 (N=20) 28mg (N=16) 50mg (N=17) 70mg (N=15) Relative Reduction in Liver Fat ≥30% 10% 100% ** 100% *** 100% *** ≥50% 5% 69% ** 100% *** 93% *** ≥70% 5% 50% * 53% ** 80% *** Normalization of Liver Fat Content ≤5% 5% 25% * 53% ** 67% *** 1 A single placebo responder lost 25 pounds over 16 weeks (11% weight reduction) * p<0.05, ** p<0.01, *** p<0.001 versus placebo (ANCOVA)

- CONFIDENTIAL - EXPANDING EFX TO CIRRHOTIC PATIENT POPULATION (F4) Developing Treatments for Cirrhotic (F4) NASH • FDA draft guidance specific for F4 patients • Projected ~3.5M US F4 patients in 2030 • FDA: The goals of treatment for compensated NASH cirrhosis are to halt or slow progression of fibrosis, prevent clinical decompensation, reduce the need for liver transplantation, and improve survival 38

- CONFIDENTIAL - 39 CIRRHOSIS REGRESSION IS ASSOCIATED WITH IMPROVED CLINICAL OUTCOMES Pooled treatment groups from STELLAR 4 and s imtuzumab cirrhosis study 7.2 8.3 1.1 0.7 0 1 2 3 4 5 6 7 8 9 NASH CRN fibrosis stage Ishak fibrosis stage No fibrosis regression Fibrosis regression 69/957 69/834 2/176 2/300 Liver - related events (%) Hazard Ratio: 0.16 p=0.0104 Hazard Ratio: 0.08 p=0.0004 Cirrhosis regression observed in 16% of patients (treatment and placebo groups) over 48 weeks Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. No head - to - head clinical trials have been conducted. Sanyal A, et al. AASLD TLMdX2020. #90

- CONFIDENTIAL - -10 -8 -6 -4 -2 0 CFB -10 -8 -6 -4 -2 0 CFB REDUCTIONS IN MARKERS OF LIVER INJURY (F4 NASH) LS Mean Change from Baseline to Week 16 ** p<0.01, versus placebo (ANCOVA) Placebo EFX 50mg ALT (U/L) Placebo EFX 50mg AST (U/L) ††† p<0.001, versus baseline (ANCOVA) Source Data: Full Analysis Set, F4; Topline preliminary data - 10.3 ** - 1.3 - 9.6 ††† - 4.5 40 n =20 n=10 n =20 n=10

- CONFIDENTIAL - LDL Cholesterol -10% -5% 0% 5% 10% 15% 20% 1 Placebo EFX 50mg - 8% +16% ** IMPROVED LIPOPROTEIN PROFILE (F4 NASH) 41 LS Mean Change From Baseline to Week 16 (%) ** p<0.01, versus placebo (ANCOVA) Source Data: Full Analysis Set, F4 ; Topline preliminary data Triglycerides -35% -30% -25% -20% -15% -10% -5% 0% 5% 10% 1 Placebo EFX 50mg - 29% +1% ** 0% 5% 10% 15% 20% 25% 30% 35% 1 HDL Cholesterol Placebo EFX 50mg +33% +3% ** Non - HDL Cholesterol -20% -15% -10% -5% 0% 5% 10% 15% 1 Placebo EFX 50mg - 14% +12% *** ** p<0.01, versus placebo (ANCOVA) ** p<0.01, versus placebo (ANCOVA) *** p<0.001, versus placebo (ANCOVA) n =20 n=10 n =20 n=10 n =20 n=10 n =20 n=10

- CONFIDENTIAL - 0% 25% 50% 75% 100% 1 -25% -20% -15% -10% -5% 0% 1 -0.5 -0.4 -0.3 -0.2 -0.1 0.0 0.1 0.2 0.3 CFB - 0.4 +0.1 IMPROVED GLYCEMIC CONTROL; TREND TOWARD WEIGHT LOSS (F4 NASH) 42 Adiponectin 2 C - Peptide 2 LS Mean Change From Baseline to Week 16 (%) ** p<0.01, versus placebo (ANCOVA) Source Data: Full Analysis Set; Topline preliminary data 1 Absolute change from baseline, % 2 Relative percent change from baseline +95% +4% - 20% - 7% ** *** -2.5% -2.0% -1.5% -1.0% -0.5% 0.0% 0.5% 1.0% 1 + 0.9% - 2.2% Body Weight 2 2 Relative percent change from baseline 2 Relative percent change from baseline *** p<0.001, versus placebo (ANCOVA) †† †† p<0.01, versus baseline (ANCOVA) Placebo EFX 50mg Placebo EFX 50mg Placebo EFX 50mg Placebo EFX 50mg n =20 n=10 n =20 n=10 n =20 n=10 n =20 n=10 HbA1c 1

- CONFIDENTIAL - FGF21 DEVELOPMENT LANDSCAPE Noninvasive Measures: Percent Change From Baseline to End of Study Akero (EFX) 16 weeks BMS ( Pegbelfermin ) 16 weeks 89Bio (BIO89 - 100) 12 weeks Dose pbo 28 QW 50 QW pbo 20 QW 10 QD pbo 18 QW 27 QW 36 Q2W Patient Population Biopsy - confirmed NASH Biopsy - confirmed NASH 80% NAFLD ; 20% biopsy - confirmed NASH * ≥1 Stage Fibrosis Improvement and No Worsening of NASH, % of Subjects 0% 46% 62% No end - of - study biopsy No end - of - study biopsy MRI - PDFF, % relative reduction 0 - 63 - 71 - 6 - 26 - 38 +10 - 36 - 60 - 50 ALT 0 - 41 - 51 - 5 - 22 - 33 - 4 - 27 - 44 - 40 Triglycerides +6 - 39 - 48 0 - 5 - 5 - 2 - 18 - 28 - 21 HDL - C +4 +34 +39 - 2 +12 +13 +2 +9 +3 +10 LDL - C 0 - 16 - 2 +1 +1 - 11 +1 +3 - 16 - 4 Adiponectin - 8 +65 +80 - 4 +16 +15 - 4 +29 +61 +24 % HbA1c, absolute change +0.1 - 0.1 - 0.4 NR 0 +0.1 - 0.3 +0.5 NR, not reported Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. No head - to - head clinical trials have been conducted. Sanyal et al (2019) Lancet; 89Bio October 5 Corporate Presentation * Subjects with biopsy - confirmed NASH were present only in the 18mg QW & 18 Q2W cohorts (Loomba et al., 2020 AASLD Poster #LP34) 43

- CONFIDENTIAL - -20% 0% 20% 40% 60% 80% 100% -50% -40% -30% -20% -10% 0% 10% 44 PERIPHERAL FGFR1c ACTIVATION Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. No head - to - head clinical trials have been conducted. Sanyal et al (2019) Lancet; 89Bio October 5 Corporate Presentation Adiponectin EFX (Akero) 89Bio * Triglycerides BMS Change from Baseline to End of Study pbo 28 QW 50 QW pbo 18 QW 27 QW 36 Q2W pbo 20 QW 10 QD pbo 28 QW 50 QW pbo 18 QW 27 QW 36 Q2W pbo 20 QW 10 QD EFX (Akero) 89Bio * BMS * Subjects with biopsy - confirmed NASH were present only in the 18mg QW & 18 Q2W cohorts (Loomba et al., 2020 AASLD Poster #LP34) Change from Baseline to End of Study

- CONFIDENTIAL - 45 FGF21 DEVELOPMENT LANDSCAPE: SUMMARY Consideration Fc - FGF21 Fusion Protein (Akero) Pegylated FGF21 (BMS or 89Bio) Patient Population: NASH diagnosed only by biopsy; NASH patients have more advanced disease and worse comorbidities Biopsy - confirmed NASH BMS: biopsy - confirmed NASH; 89Bio: ~20% biopsy - confirmed NASH * Histology: Fibrosis only histological endpoint correlated with liver outcomes Demonstrated fibrosis improvement by histology BMS: histology data pending 89Bio: no histology data Liver Fat Reduction: Max reduction requires inhibition of both hepatic fat synthesis and adipose tissue lipolysis 71% (50mg QW) BMS: 38% (10mg QD) 89Bio: 60% (27mg QW * ) Liver Enzymes (LFTs): Reductions indicate improved liver health Large reductions in LFTs; Consistent dose response BMS/89Bio: Smaller effects on LFTs Lipids: Cardiovascular risk #1 cause of mortality for NASH patients. Reflects liver and adipose effects Robust and consistent TG and HDL - C effects BMS/89Bio: Smaller effects on TG and HDL - C Glycemic Control: Improvement in HbA1c mediated by peripheral insulin sensitization; 50% NASH patients diabetic Significant decrease in HbA1c BMS: HbA1c not reported 89Bio: no significant change in HbA1c Safety & Tolerability: Baseline patient population influences profile; Mild GI events common for FGF21 in NASH patients In line with FGF21 class BMS: In line with FGF21 class 89Bio: ~80% NAFLD * EFX delivered numerically largest effects, a clear dose response, with maximal or near - maximal effect at 50mg QW * Subjects with biopsy - confirmed NASH were present only in the 18mg QW & 18 Q2W cohorts (Loomba et al., 2020 AASLD Poster #LP34)

A Global Disease, A Pioneering Treatment NASDAQ: AKRO