Exhibit 99.1

Aramchol ™ Treating NASH through prevention and reversal of fibrosis January 2018

“Safe Harbor” and Disclaimer Statement This presentation contains forward - looking statements about our expectations, beliefs or intentions regarding, among other thing s, our product development efforts, business, financial condition, results of operations, strategies or prospects. In addition, from time to time, we or our representatives have mad e o r may make forward - looking statements, orally or in writing. Forward - looking statements can be identified by the use of forward - looking words such as “believe,” “expect,” “intend,” “plan,” “may,” “should” or “anticipate” or their negatives or other variations of these words or other comparable words or by the fact that these statements do not relate str ict ly to historical or current matters. These forward - looking statements may be included in, but are not limited to, this presentation, various filings made by us with the SEC, press rele ase s or oral statements made by or with the approval of one of our authorized executive officers. Forward - looking statements relate to anticipated or expected events, activities, trends or results as of the date they are made. Because forward - looking statements relate to matters that have not yet occurred, these statements are inherently subject to risks and uncerta int ies that could cause our actual results to differ materially from any future results expressed or implied by the forward - looking statements. Many factors could cause our actual activities o r results to differ materially from the activities and results anticipated in forward - looking statements, including, but not limited to, the factors summarized below. These factors include, but are not limited to, the following: the timing and cost of Galmed's ongoing Phase IIa ARRIVE Study, Phase IIb ARREST Study, and planned Phase III trials for Aramchol™, or whether Phase III trials will be conducted at all; completion and receiving favorable results of these Phase IIa ARRIVE Study, Phase IIb ARREST Study and Phase III trials for Aramchol™; regulatory action with respect to Aramchol™ by the FDA or the EMA; the commercial launch and future sales of Aramc hol ™ or any other future products or product candidates; Galmed's ability to comply with all applicable post - market regulatory requirements for Aramchol™ in the countries in which it seeks to m arket the product; Galmed's ability to achieve favorable pricing for Aramchol™; Galmed's expectations regarding the commercial market for NASH in patients who are overweight or obese and have pre diabetes or type I I diabetes mellitus; third - party payor reimbursement for Aramchol™; Galmed's estimates regarding anticipated capital requirements and Galmed's needs for additional financing; market adoption of Aramchol™ by physicians and patients; the timing, cost or other aspects of the commercial launch of Aramchol™; th e d evelopment and approval of the use of Aramchol™ for additional indications or in combination therapy; and Galmed's expectations regarding licensing, acquisitions and strategic operations. More detailed information about the risks and uncertainties affecting Galmed is contained under the heading "Risk Factors" included in Galmed's most recent Annual Report on Form 20 - F filed with the SEC on March 23 , 2017 , and in other filings that Galmed has made and may make with the SEC in the future. These statements are only current predictions and are subject to known and unknown risks, uncertainties and other factors tha t m ay cause our or our industry’s actual results, levels of activity, performance or achievements to be materially different from those anticipated by the forward - looking statements. Given these uncertainties, you should not rely upon forward - looking statements as predictions of future events. All forward - looking statements attributable to us or persons acting on our behalf included in, but not limited to, this presenta tion speak only as of the date hereof and are expressly qualified in their entirety by the foregoing. We undertake no obligations to update or revise forward - looking statements to refl ect events or circumstances that arise after the date made or to reflect the occurrence of unanticipated events. In evaluating forward - looking statements, you should consider these r isks and uncertainties. 2

Overview Scientific Rationale Clinical Data Corporate Overview

Galmed Snapshot Aramchol™ demonstrates anti - steatosis and anti - fibrotic effects consistently in all pre clinical models ( in - vitro and in - vivo ) 4 Galmed is advancing its lead compound, Aramchol™ towards registration with a focus on NASH SteatoFibrosis , a market opportunity estimated to reach $35 - 40B/ yr by 2025 Experienced pharma leadership team • ARRIVE topline data Q 1 2018 • ARREST topline data Q 2 2018 • Pre - Phase 3 meeting with the FDA Q 4 2018 • Efficacy in animals translated to efficacy in patients in Phase IIa study • ARREST Phase IIb NASH study is based on a successful Phase IIa with a similar primary end - point Expected Short Term Catalysts:

Aramchol ™ – NASH Disease Modification Potential 5 Fast Track Designation for development of Aramchol ™ for NASH granted by FDA First - in - class, orally active, liver targeted SCD - 1 modulator Effects in animal models translated into human clinical data High safety margin and B/R ratio ~ 400 subjects exposed across 7 clinical trials Potent mechanism with multiple intervention points along the pathogenic pathway

Seasoned Management Team Guy Nehemya , Adv., MBA, VP Operations Yael Hollander, Adv .,MBA , VP, Legal Affairs & Strategy Yohai Stenzler , CPA , MBA , CFO + 10 years of experience, Senior Clinical Program Leader at Teva Pharmaceuticals Dr. Tali Gorfine , M.D., CMO + 16 years of experience in drug development, Teva Pharmaceuticals Dr. Liat Hayardeny , Ph.D., MBA, CSO Allen Baharaff , President and CEO Co - founder of Galmed + 6 years of financial management experience at Ernst & Young LLP + 6 years of experience at Gross, Kleinhendler , Hodak , Halevy, Greenberg & Co. +4 years of experience as the Company's Director of Operations. Chaim Hurvitz CEO of CH Health; Previously, member of Teva’s senior management team and Board of directors. Carol L. Brosgart, M.D. Consultant to biotechnology companies in the areas of liver disease; Former director of Tobira Therapeutics. William S. Marth President & CEO of Albany Molecular Research Inc. (AMRI) ; former President & CEO of Teva in the Americas. David Sidransky, M.D. Professor of Oncology Pathology at John Hopkins University. Ran Oren, M.D. Head of the Institute of Gastroenterology and Liver Disease at Hadassah Ein Kerem Hospital. Tali Yaron - Eldar Formerly Israeli Tax Commissioner; Chief Legal Advisor of the Finance Ministry of the State of Israel. Shmuel Nir President & CEO of Tushia Consulting Engineers Ltd.; Chairman of the Board of Directors of Matan Digital Printers Ltd. Allen Baharaff BOARD OF DIRECTORS LEADERSHIP + 34 years of CMC experience, former Chief Scientific Officer at Chemagis (Perrigo API) Yossi Caspi , Ph.D., Senior Director Drug Development

Overview Scientific Rationale Clinical Data Corporate Overview

8 Metabolism (Steatosis) Cell stress Apoptosis Collagen Production (Fibrosis) Inflammation Metabolism (Steatosis) Vitamin E CCR 2 - CCR 5 Galectin ARAMCHOL™ De - compensated Cirrhosis/ HCC Pathophysiology of NASH ASK 1 Caspase PPARs GLP - 1 FXR FGF 21 SCD 1 Aramchol™ Reduces Key Pathologies Pathways of NASH

Hepatology 2003 ; 38:436 - 442 Archives of Biochemistry and Biophysics 471 ( 2008 ) 63 – 71 European Journal of Gastroenterology & Hepatology 2008 , 20:1205 – 1213 Archives of Medical Research 41 ( 2010 ) 397 - 404 9 Data Demonstrating Beneficial Effect of Aramchol™ on NASH

MCD 0.1 % Diet н Aramchol™ 5 mg/kg MCD 0.1% Diet MCD diet model is one of the most commonly used animal models of NASH, as it induces a liver pathology that resembles the sequence and progression of liver pathology seen in human. 10 52.6 % 86.4 % 79 % Iruarrizaga-Lejarreta , Marta, et al. "Role of Aramchol in steatohepatitis and fibrosis in mice. "Hepatology Communications 1.9 ( 2017 ): 911 - 927 . Data Support Improvement in Liver Steatosis & Inflammation Normal Diet

Collagen extract from livers of MCD diet mice treated with Aramchol Control MCD 0.1 % MCD 0.1 % +A ramchol™ 5 mg/kg Collagen Type 1 11 Iruarrizaga-Lejarreta , Marta, et al. "Role of Aramchol in steatohepatitis and fibrosis in mice. "Hepatology Communications 1.9 (2017): 911 - 927. 43.5 % 38 % Data Support Improvement in Liver Fibrosis MCD 0.1 % Diet н Aramchol™ 5 mg/kg MCD 0.1 % Diet Normal Diet

12 TAA + A ramchol™ 5 mg/kg TAA No Treatment Fibrosis Score (Masson & Goldner staining) 40 % Data Support Direct Effect on Prevention of Liver Fibrosis Effect in the TAA model is considered to best predict efficacy in human R. Golan - Gerstl 1 , M. Valitsky 1 , R. Oren 1 , E. Brazovski 2 , L. Hayardeny 1 , S. Shimon Reif . "The anti - fibrotic effect of Aramchol on liver fibrosis in TAA animal model" ( 2017 ); The international liver congress (EASL), Amsterdam, the Netherlands.

MoA Suggesting Major Role of Aramchol™ in Fibrosis Cell number – Methylenblue (OD 620 nm) Relative Absorption COL 1 A 1 mRNA expression (a. u.) Stellate Cell Collagen Production – mRNA Stellate Cell Proliferation – Cell Number 58.9 % 41 % 13 Aramchol™ - Unique MoA to Show Effect on Collagen Producing Cells in the Liver

14 • The generation of ROS is well - known to play an important role in producing liver injury and initiating hepatic fibrogenesis . • ROS damages lipids, proteins and DNA, induces necrosis and apoptosis and amplifies the inflammatory response, all key factors in fibrogenesis . • Among the arsenal of antioxidants existing in the cell, glutathione (GSH) is the most important to neutralize the damaging activity of ROS and maintain redox homeostasis. Dobrzyn , Pawel, et al. " Stearoyl - CoA desaturase 1 deficiency increases fatty acid oxidation by activating AMP - activated protein kinase in liver." Proceedings of the National Academy of Sciences of the United States of America 101.17 ( 2004 ): 6409 - 6414 .

Overview Scientific Rationale Clinical Data Corporate Overview

A Phase 2 , Multicenter, Double - blind, Randomized, Placebo - Controlled Study on the Effect of Aramchol™ on Liver Triglycerides Concentration in Patients with Steatosis due to Non Alcoholic Fatty Liver Disease (NAFLD) or Non Alcoholic Steatohepatitis (NASH)* 1 6 Study Arms 300 mg; 100 mg; Placebo Treatment Plan Once - daily tablet for 12 weeks and 4 weeks follow - up No. of Subjects N=60 Primary Endpoints % change in the liver triglycerides concentration measured by MRS Secondary Endpoints Liver and metabolic biomarkers level Phase IIa Completed More information about the Phase IIa study may be found on ClinicalTrials.gov (identifier: NCT 01094158 ); this study has been completed.

Phase IIa Efficacy and Safety Overall and most frequent events ( > 2 patients in any group) Percent relative change in liver TG levels, baseline and end of treatment Aramchol 300 mg N = 20 n (%) Aramchol 100 mg N = 20 n (%) Placebo N = 20 n (%) Patients with AE(s) 9 (45.0) 8 (40.0) 11 (55.0) Preferred term Abdominal pain 1 (5.0) 1 (5.0) 2 (10.0) Abdominal upper pain 2 (10.0) 1 (5.0) Back pain - - 3 (15.0) Constipation - - 2 (10.0) Asthenia - - 2 (10.0) Upper respiratory tract infection 2 (10.0) - - 300 mg Aramchol TM demonstrated statistically significant liver fat content reduction • Similar frequency of adverse events in all treatment groups • Adverse events were mild or moderate, none were serious • None of the patients withdrew as a result of adverse events Safadi R, Konikoff FM, et al. "The fatty acid – bile acid conjugate aramchol reduces liver fat content in patients with nonalcoholic fatty liver disease." Clinical Gastroenterology and Hepatology 12.12 ( 2014 ): 2085 - 2091 .

ARREST – AR amachol™ for RE solution of ST eatohepatitis A Phase IIb, double blind randomized, controlled clinical trial, to evaluate the efficacy and safety of two Aramchol TM doses versus placebo in patients with Non - Alcoholic Steatohepatitis 18 Design: Multicenter, randomized, double - blind, placebo - controlled, dose ranging study Participants: Biopsy - diagnosed (centrally read) NASH patients with obesity and insulin resistance Doses: • 2:2:1 • ~100 patients 600mg; 100 patients 400mg; 50 patients placebo Treatment Plan: • 12 months treatment (once - daily tablet) and 3 months of follow - up Number of Subjects: 2 ϰϴ patients  Primary Endpoint: % change in the liver triglycerides concentration measured by MRS Main Secondary Endpoints: • Proportion (%) of subjects with CRN Fibrosis Score Improvement without worsening of NASH • Proportion (%) of subjects with NAS Score Improvement (>=2 points) without worsening of CRN Fibrosis Score • Proportion (%) of subjects with NASH Resolution (ballooning 0; inflammation 0 or 1) without worsening of CRN Fibrosis Score More information about the ARREST study may be found on ClinicalTrials.gov NCT 02279524 ); this study is ongoing but not recruiting participants; results are expected Q 2 2018

AR R EST Baseline Histolog y  70% of patients have NAS > 5 60 % of patients have fibrosis stage 2 and 3 3 % 36 % 20 % 40 % 1% 0 1 2 3 4 30 % 41% 19 % 8 % 2 % 4 5 6 7 8 NAS score NAS = NAFLD Activity Score, ranges from 0 - 8 and is composed of the unweighted sum of three histological components: steatosis ( 0 - 3 ), lobular inflammation ( 0 - 3 ) and ballooning degeneration ( 0 - 2 ) The Clinical Research Network (CRN) Pathology Committee developed a scoring system using NASH activity (Grade) and collagen deposition plus architectural remodeling (Stage) ARREST enrolled a population with advanced NASH with fibrosis that is expected to enable a pivotal study with a single dose and optimized primary end point CRN fibrosis stage 19

What About Combinations? ✓ Aramchol ™ is an ideal candidate for combination treatment Fibrotic NASH is a complex disease resulting from the interplay of numerous, interconnected damage pathways. Combination therapies are justified by complimentary MoA’s: • metabolic • inflammatory • fibrotic 20 Aramchol™, with its unique MoA and excellent safety and tolerability profile is complimentary to all clinical programs under development: • Metabolism (All FXR’s) • Cell stress and apoptosis • Anti inflammatory • Anti fibrotic via other mechanisms

Aramchol TM versus placebo in the treatment of HIV - associated nonalcoholic fatty liver disease and lipodystrophy : A randomized, double - blinded, allocation - concealed, placebo controlled clinical trial . An investigator - initiated study conducted at the NAFLD Research Center, University of California San Diego by Professor Rohit Loomba . ARRIVE – AR amchol TM for the R eversal of H IV - Associat E d Lipodystrophy and NAFLD 21 Design: Single center, randomized, double - blind, placebo - controlled, proof of concept Participants: Patients with HIV - associated NAFLD Doses: • Placebo (25 patients) • 600 mg (25 patients) Treatment Plan: Once - daily tablet for 12 weeks Number of Subjects (Est.) : 50 patients Primary Endpoint: Hepatic steatosis assessed by MRI - PDFF Secondary Endpoints: MRE, Total body fat, metabolic profile, and liver biochemistry More information about the ARRIVE study may be found on ClinicalTrials.gov NCT 02684591 ); this study is ongoing but not recruiting participants; results are expected Q 1 2018

Overview Scientific Rationale Clinical Data Corporate Overview

Corporate Overview s Financial Ownership Structure ( 1 ) Intellectual Property • 16 Patent Families • Areas of Focus: NASH, Combinations, Chemistry of Aramchol™, New Indications • Patent family (WO 2002 / 2083147 ) for use of Aramchol ™ for the treatment of fatty liver granted worldwide. • 2 US Provisional patent applications directed to the use of Aramchol™ for treating fibrosis. Once granted will expire on 2037 . • Market Cap $ 132 M ( 1 ) • 14.4 M Outstanding shares ( 1 ) • Cash Items - ~$ 19.0 M ( 1 )( 2 ) • No debt • NASDAQ: GLMD ( 1 ) Company estimate as of 12 / 31 / 17 ( 2 ) Unaudited, consisting of cash, cash equivalents and marketable securities. Top 5 Institutional Holders: • 683 Capital Management LLC • Park West Asset Management • Man GLG LLC • Sphera Funds Management Ltd. • Meitav Dash Gemel Retail 43 % Institutional 15 % Insiders & Others 42 %

Estimation of 2025 NASH D rug - T reated P atient P opulation (US+EU 5 ) Description/Assumptions Source Value Driver Adult pop . size of countries EU 5 & US ; Linear yearly pop . growth rates 2013 to 2035 ; Adult pop . ( 20 - 70 years) is only relevant age group Intl. Diabetes Federation + 0.14 %  p.a. Population size 1 Prevalence of metabolic syndrome in EU - 5 and US ; Forecast of change in prevalence is same as in obesity Earl et. al - JAMA 26 % + 0.8 % p.a. Prevalence of metbolic syndrome 2 Prevalence of NAFLD 3 in met. syndrome patients times prevalence of NASH patients in NAFLD patients who have metabolic syndrome Assuming that all patients undergoing bariatric surgery have metabolic syndrome Ratziu et. al. - J Hep. 2012 / 2010 45 % NASH share of met. syndrome patients 3 Of prevalent NASH population only a share is identified in clinical practice by having elevated liver enzymes, ultrasound, sy mpt oms and then referred to a physician who diagnoses NASH KOL interviews (Hepatologists) 25 - 50 % Diagnosis rate 4 Rate of resistance of NASH patients to effectively respond to a 3 - 6 month lifestyle intervention ( 5 - 10 % weight loss with improvement of clinical and diagnostic parameters) KOL interviews (Hepatologists) 80 % Resistance to life - style intervention 5 Number of Patients taking pharmacologic treatment for NASH ; French treatment rate valid for all other countries Ratziu et. al. - J Hep. 28 - 50 % Drug treatment rate 6 470 M 122 M 55 M 16 M 6 M 2025 total (US+EU 5 ) : 21 M 100 % 26 % 11.6 % 3.5 % 1.2 % 4.4 % Population  per country  (adult) - 240 M US - 230 M EU - 5 People with metabolic syndrome People affected by NASH NASH patients resistant to lifestyle intervention Patients treated with drug NASH patients diagnosed in NASH population 24

5 Key Takeaways About Galmed 25 Experienced leadership Data from Phase IIa ARRIVE Study and Phase IIb ARREST Study expected in Q 1 & Q 2 2018 , respectively The effect on steatosis has been demonstrated in humans in a Phase IIa study with a significant reduction in liver fat demonstrated by MRS Aramchol™ has shown a significant effect on the 3 key pathologies of NASH (steatosis, inflammation and fibrosis) in several pre - clinical models The effect on fibrosis is both indirect, through reduction of steatosis, and direct through reducing stellate cell proliferation and collagen production

Thank you ! NASDAQ: GLMD

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