Exhibit 99.1
Pioneering Innovative Treatments for Fibrotic DiseasesCorporate Overview | Non-Confidential | November
2021
Forward Looking Statements This presentation contains "forward-looking statements" within the meaning
of the Private Securities Litigation Reform Act. These forward-looking statements include, among other things, statements regarding the clinical development pathway for CM-101; the future operations of Chemomab and its ability to successfully
initiate and complete clinical trials and achieve regulatory milestones; the nature, strategy and focus of Chemomab; the development and commercial potential and potential benefits of any product candidates of Chemomab; and that the product
candidates have the potential to address high unmet needs of patients with serious fibrosis-related diseases and conditions. Any statements contained in this communication that are not statements of historical fact may be deemed to be
forward-looking statements. These forward-looking statements are based upon Chemomab’s current expectations. Forward-looking statements involve risks and uncertainties.Because such statements deal with future events and are based on
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presentation, including: the uncertain and time-consuming regulatory approval process; risks related to Chemomab’s ability to correctly manage its operating expenses and its expenses; Chemomab’s plans to develop and commercialize its product
candidates, including CM-101; the timing of initiation of Chemomab’s planned clinical trials; the timing of the availability of data from Chemomab’s clinical trials; the timing of any planned investigational new drug application or new drug
application; Chemomab’s plans to research, develop and commercialize its current and future product candidates; the clinical utility, potential benefits and market acceptance of Chemomab’s product candidates; Chemomab’s commercialization,
marketing and manufacturing capabilities and strategy; Chemomab’s ability to protect its intellectual property position; and the requirement for additional capital to continue to advance these product candidates, which may not be available on
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Discovery and development of innovative therapeutics for rare inflammatory and fibrotic diseases with
high unmet need CM-101, a first-in-class CCL24 neutralizing monoclonal antibody targeting:Primary Sclerosing Cholangitis (PSC)Systemic Sclerosis (SSc)Liver fibrosis (MoA*) Conducting 2 Phase 2 clinical trials with 3rd Phase 2 trial expected
to initiate in 1Q22First clinical readouts targeted for 2022 expected to drive multiple value inflections Global patent exclusivity through 2041. Granted composition of matter patent with multiple additional patents pending. Investment
Highlights Clinical Stage Biotech Company Focused on Inflammatory-Fibrotic Diseases Cormorant Asset Management Cash and equivalents of $67M as of June 30, 2021, enabling runway through mid-2023 Focus CM-101:A Pipeline in A
Product Near-Term Catalysts Robust IP Portfolio Top Tier Investors Solid Balance Sheet *MoA – Mechanism of Action
Experienced Management ARNON AHARON, MDChief Medical Officer DALE PFOST, PhD Chief
Executive Officer SHARON ELKOBIVP Business Development MICHAL SEGAL-SALTO, PhDVP Research and Development DON MARVINChief Financial Officer, EVP and COO ADI MOR, PhDCo-founder & Chief Scientific Officer
Stephen Squinto, PhD Chairman of the Board Adi Mor, PhDCo-founder & Chief Scientific Officer Dale
Pfost, PhD Chief Executive Officer Neil Cohen, MADirector Nissim Darvish, MD, PhDDirector Joel Maryles, CFA, MBADirector Alan Moses, MD Director Claude Nicaise, MDDirector Board of Directors Scientific Advisory Board (partial) Prof.
Marco Matucci-Cerinic, MD, PhDDirector of the Division of Rheumatology, University of Florence, Italy Scott L. Friedman, MDDean for Therapeutic Discovery and Chief, Division of Liver Diseases, Mount Sinai, NY, USA Prof. Dinesh Khanna MD,
MBBS, MScDirector of the Scleroderma Program, University of Michigan, Ann Arbor, Michigan, USA Massimo Pinzani, MD, PhD, FRCP Sheila Sherlock Chair of Hepatology, Director UCLInstitute for Liver and Digestive Health, RFH, London, UK Gideon
Hirschfield, MA MB PhDLily and Terry Horner Chair in Autoimmune Liver Disease, University of Toronto, Toronto General Hospital, Canada Prof. Francesco Del Galdo, MD, PhDHead of the Scleroderma Program at NIHR, University of Leeds,
UK Experienced Leadership
Program Indication Target Discovery Preclinical Phase 1 Phase 2 Status CM-101 Primary
Sclerosing Cholangitis CCL24 Enrolling PatientsTop Line Data 2H 2022 CM-101 Systemic Sclerosis CCL24 Initiation Expected In 1Q 2022 CM-101 Liver Fibrosis (MoA*) CCL24 Enrolling PatientsTop Line Data 1H
2022 Next-gen Fibrosis Screening In Progress CM-101: Pipeline in a Product Addressing Fibrotic Diseases with High Unmet Need Orphan designation granted from FDA and EMA Orphan designation granted from FDA and EMA Mechanism
of Action & SC Route of Administration (in NASH patients) *MoA – Mechanism of Action
CCL24 is a Novel Therapeutic Target for Fibrosis Critical Mediator Promoting Inflammation and
Fibrosis CCL24 CCR3 CCL24-regulated cellsFibroblasts (liver, lung and skin), Immune and Epithelial cells Immune cell recruitment Fibroblast activation Tissue scarring, inflammatory-mediated damage, collagen deposition Positive
Feedback Loop Organ failure Damaged tissue CCL24 Secretion CCL24-secreting cellsImmune (M2 Macrophages, monocytes) and Epithelial cells Dual role in promoting fibrosisdirectly activates fibroblastsenhances local immune cell
recruitmentUnique and differentiated activityex vivo and in vivo data confirms unique role vs other CCLscorrelates with disease outcome and fibrotic biomarkers Minor expression in healthy tissuesignificantly elevated in liver, skin, lung
fibrotic tissue wide therapeutic marginPositive feedback loop potentiates tissue damageresponsible for initiation and perpetuation of fibrosis
CCR3 Immune cell recruitment Fibroblast activation &
proliferation CCL24 CM-101 Fibrosis Inflammation CM-101: A First-in-Class mAb Blocking CCL24 Dual Mechanism of Action Interfering with the Core Fibrotic Pathways CM-101 attenuates inflammation and fibrosis by inhibiting
fibroblast activation and immune cell recruitment CM-101 Inhibits Primary Hepatic Fibroblast Activation CM-101 Reduces In-vivo Monocyte Recruitment
Strong Preclinical Evidence of CM-101 via CCL24 Inhibition Significant Attenuation of Fibrosis
& Inflammation Across a Wide Range of Models Primary sclerosing cholangitisANIT induced cholestasis-chronic and acute (mice)Bile duct ligation (rat)MDR2 knock-out (mice)Systemic sclerosisBleomycin-induced skin fibrosis (mice)Bleomycin
induced lung fibrosis (mice)Liver FibrosisTAA induced liver fibrosis (rat and mice)Liver metabolism and inflammationSTAM (mice)MCD diet induced NASH (mice)AtherosclerosisApoE knock out model (mice) Proof of Concept\Animal Models Mechanism
of Action Ex-Vivo (Patient Samples)Primary sclerosing cholangitisBiomarker correlationsOverexpression of CCL24 and CCR3Systemic SclerosisFibrotic biomarkers correlationDisease deterioration correlationOverexpression of CCL24 and CCR3 Liver
Fibrosis (NASH)Disease severity correlationOverexpression of CCL24 and CCR3In-Vivo (Knockout Animal Models)Systemic SclerosisCCL24 knock out vs. WT in Bleomycin induced skin fibrosis model (mice)Liver metabolism and inflammation CCL24
knockout vs. WT in MCD-induced NASH (mice) CCL24 Target Validation Short-term GLP in rodentsLong-term GLP in Non-human primatesEx-vivo safety: ADCC, CDC, cytokine secretionTissue cross reactivity Toxicology CM-101 effects on fibroblast
activationDermal, Hepatic and Lung fibroblast activationDermal and liver fibroblast transition to myofibroblastsHepatic fibroblast motilityCM-101 effects on immune cells migration and recruitmentDermal fibroblast migrationMonocyte
polarizationMonocyte recruitment
Double-Blind, Randomized Escalating Dose (N=32) CM-101 0.75 mg/kg IV or placebo (n=8) CM-101 2.5
mg/kg IV or placebo (n=8) CM-101 5 mg/kg IV or placebo (n=8) CM-101 10 mg/kg IV or placebo (n=8) Double-Blind, Randomized Single Dose (N=8) CM-101 5 mg/kg SC or placebo (n=8) IV Phase I End of 42 days follow-up period SC Phase
I End of 42 days follow-up period Screening period (up to 28 days) Follow-up period (6 weeks) n=40 healthy volunteers Phase Ia Results CM-101 was safe and well tolerated at all tested doses up to 10 mg/kg and for both formulations
All drug related AEs were classified as mild with no SAEs reportedAverage half-life of 19-21 days (for IV and SC), supports long interval administration once every 2-4 weeksDose-dependent target engagement measured by serum CCL24
levelsComparable target engagement & PK profiles for the SC and IV formulations IV - Intravenous; SC - Subcutaneous Single Ascending Dose Study Shows CM-101 to be Safe and Well Tolerated in Healthy Volunteers
Wk 15End of treatment Wk 18End of study Double-Blind, Randomized Escalating Dose (N=16) CM-101
2.5 mg/kg IV or placebo (n=8) CM-101 5 mg/kg SC or placebo (n=8) Phase Ib Day 0Randomization Study population: NAFLD patients with normal liver functionMultiple CM-101 administrations were safe and well tolerated using both IV and SC
formulationsMost frequently reported AEs were mild with no drug-related SAEs reportedFavorable t1/2, supports long dosing interval (Q2W - Q4W) Phase Ib Results Multiple Administration Study Showed CM-101 to be Safe & Well Tolerated in
NAFLD Patients IV - Intravenous; SC – Subcutaneous; Wk - week Study Design Tested doses - 2.5 mg/kg IV infusion and 5 mg/kg SC injection 5 repeated administrations per patient; Q3WPrimary endpoint - safety and tolerability
Phase Ib: Confirms CM-101 Anti-Fibrotic Mechanism in Humans Demonstrated Biomarker Improvement
with Dose-Dependent PK-Target Engagement PK-Target Engagement PK-PD 2.5mg/kg IV PK-PD 5mg/kg SC Liver Stiffness Relative change from baseline (%) Nordic Biosciences , Denmark Fibrotic Biomarkers
Improved* FibroScan™ ProC4 *Concordant results across 6 relevant fibrotic markers TIMP1 ElastographyDecreased Relative change from baseline (%) EOT EOT ProC4-Procollagen 4TIMP1-Tissue inhibitor of metallopeptidase 1EoT-End of
Treatment
CM-101 for the Treatment of Primary Sclerosing Cholangitis
Source: Johns Hopkins Medicine Primary Sclerosing Cholangitis (PSC) PSC is a rare, chronic liver
disease characterized by progressive course of cholestasis with inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts leading to end-stage liver disease and cirrhosisDiagnosis is most often between the age of 30 and 40
years; Predominantly affect men (2:1 male:female ratio)No FDA approved drug; Liver transplant is the only therapy with curative potentialMedian Survival of 10-12 years with no intervention~77K patients in 7 major markets Lazaridis et al.
Primary Sclerosing Cholangitis., N Engl J Med. 2016 James H et al.Primary Sclerosing Cholangitis, Part 1: Epidemiology, Etiopathogenesis, Clinical Features, and Treatment Gastroenterology & Hepatology 20187 Major Markets – USA, 5EU (UK,
Germany, France, Italy, Spain), Japan Characterized by High Morbidity and Mortality
CCL24 serum level in PSC patients Healthy Liver Collaboration with RFH, UK PSC
Liver CCL24 STAINING CCL24 expression is significantly and selectively elevated in PSC livers CCL24 level in healthy vs PSC patients' livers tissues CCL24 correlates with ELF in PSC patients with elevated ALP CCL24 Plays a Key Role in
PSC Clinical Relevance of CCL24 in PSC Pathophysiology is Supported by Patient Samples ELF – Enhanced Liver Fibrosis; ALP – Alkaline Phosphatase CCL24 overexpressed in bile epithelial cells Enhanced Liver Fibrosis (ELF) test reflects
fibrosis and predicts clinical outcomes in PSC1 1. M. Vesterhus et al. Hepatology, 62 (1) (2015), pp. 188-197 CM-101 MoA guided the selection of ELF and ALP as primary endpoints in Phase II
% Fibrosis (sirius red staining) 82% reduction Col1A1Col3A1TIMP1ACTA2TGF-β ALTASTALP Liver
enzymes Pro-fibrotic genes CM-101 Reduces Liver Fibrosis by 82% Segal-Salto et al, JHEP reports 2020TAA- Thioacetamide Reduced Liver Collagen in TAA Liver Fibrosis Rat Model Using Therapeutic Design HEALTHY TAA SIRIUS RED
(COLLAGEN) TAA+ CM-101
CM-101 Ameliorates Liver Injury and Fibrosis in PSC Cholestasis, Inflammation and Fibrosis are
Reduced in the MDR2 Knockout Model in Mice Macrophages (IBA1) Mdr2 -/- + CM-101 Cholangiocytes (panck) Sirius Red Mdr2 -/- Mdr2 -/- Reduced Macrophage Number Mdr2 -/- + CM-101 Mdr2 -/- Mdr2 -/- + CM-101 CM-101 interferes with
the core pathways that drive PSC Decreased Bile Epithelial Cell Proliferation Attenuated Liver Collagen Deposition
Phase 2 Trial in Primary Sclerosing Cholangitis Enrolling Patients; Orphan Drug Designation Granted by
FDA and EMA Key inclusion/exclusion criteria: Primary endpoints: Serum alkaline phosphatase - change from baseline to W15ELF score - change from baseline to W15 Secondary endpoints: Fibrotic biomarkers and liver enzymes, e.g., AST, ALT,
Pro-C3, Pro-C5 - change from baseline to W15 PK, Anti-Drug AntibodyPD parameters Adults with large duct PSC of more than 24 weeks duration diagnosed via MRCP/ERCPALP > 1.5 ULNStable IBD is allowed Stable Ursodeoxycholic Acid (UDCA)
treatment is allowed No cirrhosis of liverNo liver transplantation Clinicaltrials.gov: NCT04595825 Territories: US, UK, Germany, Spain, Israel Number of sites: ~45 First data readout expected 2H2022
CM-101 for the Treatment of Systemic Sclerosis
Systemic Sclerosis (SSc) Rare autoimmune rheumatic disease characterized by inflammation and
fibrosis of the internal organs as well as vasculopathyAge of diagnosis 30-50 years, Predominantly affects women (3:1 female:male ratio)There is no approved disease modifying drug; Treatments focus on managing disease symptoms (Nintedanib,
Tocilizumab)Median Survival of 10 years - the highest mortality rate among the systemic rheumatic diseasesPulmonary involvement is the leading cause of death~170K patients in 7 major markets Global data; Bergamasco et al., Clin Epidemiol.
2019; 11: 257–2737 Major Markets – USA, 5EU (UK, Germany, France, Italy, Spain), Japan Most Lethal Among Systemic Rheumatic Diseases Source:
CCL24: A Critical Node Potentiating Systemic Sclerosis (SSc) Clinical Relevance of CCL24 in SSc
Pathophysiology is Supported by Patient Samples dSSc – diffuse systemic sclerosisMor A et al., Annals of Rheumatic Diseases, 2019***p ≤0.001 CCL24 overexpressed in skin and serum samples of dSSc Patients compared to healthyCCL24
correlates with disease progression and fibrotic biomarkers *** SSc Skin Collaboration with University of Florence Healthy Skin CCL24 serum level correlates with worsening of lung functions CCL24 is highly elevated in dSSc
population Patient samples support the targeted patient population and clinical trial endpoints
CCL24 Blockade is Singularly Sufficient to Attenuate Fibrosis Knocking Out the CCL24 Gene
Attenuates Inflammation and Fibrosis in SSc Bleomycin Experimental Model Mor A et al., Annals of Rheumatic Diseases, 2019BLM – Bleomycin; WT - Wild type; KO – Knockout, BAL- Bronchoalveolar lavage, PBS- Phosphate-buffered saline *p ≤0.05
WT-PBS CCL24 KO-PBS WT-BLM CCL24 KO-BLM Fold increase expression α SMA expression in skin lesions Dermal thickness Dermal thickness compared to average control groups * * # cells infiltrating to BAL Immune cell lung infiltration
* WT-BLM CCL24KO-BLM
CM-101 Profoundly Reduces Skin and Lung Fibrosis in SSc Experimental Models Relevant to Systemic
Sclerosis Using Prevention and Therapeutic Designs Mor et al, Annals of Rheumatoid Diseases, 2019**p ≤0.01; *p ≤0.05. BLM - bleomycin; IT - Intratracheal; SC – SubcutaneousIgG - Immunoglobulin G Attenuates skin and lung fibrosis levels in
bleomycin induced models using treatment modeDemonstrates a dose dependent attenuation of fibrosisReduces lung collagen and inflammation as compared to approved drugs for lung fibrosis Collagen concentration (µg/gr
tissue) Vehicle BLM BLM+CM-101 0.5mg/kg BLM+CM-101 1mg/kg BLM+CM-101 2.5mg/kg BLM+lgG * * ** Bleomycin (SC) induced dermal fibrosis Bleomycin (IT) induced lung fibrosis
Phase 2 Trial in Diffuse Cutaneous Systemic Sclerosis Target dcSSc patients at early stage when
disease is progressing; Primary endpoint measures holistic disease Key inclusion/exclusion criteria: Primary endpoints: Percent of participants meeting Revised CRISS criteria after 48 weeks treatmentSecondary endpoints:Change in Forced
Vital Capacity (FVC) % predicted mRSS, Health Assessment Questionnaire Disability Index, Patient and Physician Global Assessment, DLCOExploratory/Biomarker endpoints:Fibrotic biomarkers, measurement of immune cell infiltration by skin
biopsy Early systemic sclerosis diffuse subtype; within 5 years of start of symptoms Modified Rodnan skin score (mRSS) > 15 and <45Evidence of disease activity: skin and lungNo diagnosis of limited subtypeNo SSc-like illness associated
with toxic agentsNo end-stage organ involvement’ Territories: US, EU & Israel Number of sites: 100 Trial initiation expected early 2022
CM-101 Clinical Development Plan and Key Catalysts SC – Subcutaneous, MoA- Mechanism of Action
*NCT04595825 Will be Advancing in Parallel Three Phase II Clinical Programs Status 2021 2022 2023 Primary Sclerosing Cholangitis EnrollingTop line data expected in 2H2022 Systemic Sclerosis Initiation expected in
1Q2022 Liver FibrosisProof of MoA using SC formulation EnrollingTop line data expected in 1H2022 Phase II: 15 wk treatment*Randomized, placebo-controlled;US, Europe and Israel study sites Phase II: 48 wk treatmentRandomized,
placebo-controlled;US , Europe & Israel study sites Phase IIa: 16 wk treatmentRandomized, placebo-controlled;Israel study sites
Investment Summary Pioneering Innovative Treatment for Fibrosis-Related Diseases with High Unmet
Need IV – Intravenous; SC – SubcutaneousMoA – Mechanism of Action Chemomab Clinical stage company advancing PhII trials in multiple fibrotic indications with high unmet need Substantial near term value inflection pointsStrong leadership
with proven track record PK & Mode of AdministrationOptimal PK for both SC and IV formulationsComparable exposure levels and target engagement using both formulations EfficacyFirst anti-fibrotic evidence in patientsSignificant
anti-fibrotic effects across multiple in vivo, ex vivo and in vitro models CM-101First-in-class mAb blocking CCL24Novel and differentiated dual anti-fibrotic and anti-inflammatory MoA SC and IV formulations available; well established
manufacturing processStrong IP protection SafetyFavorable safety and tolerability that support chronic treatment based on toxicology, Phase Ia and Phase Ib clinical trials
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