Filed by Anchiano Therapeutics Ltd.

Pursuant to Rule 425 under the Securities Act of 1933,

as amended, and deemed filed pursuant to Rule 14a-12

under the Securities Exchange Act of 1934, as amended

Subject Company: Chemomab Ltd.

Pioneering Innovative Treatments for Fibrotic Diseases Corporate Overview | Non-Confidential | January 2021

Forward Looking StatementsThis 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 proposed merger between Chemomab and Anchiano; expectations regarding ownership structure of the combined company; the future operations of the combined company and its ability to successfully initiate and complete clinical trials and achieve regulatory milestones; the nature, strategy and focus of the combined company; the development and commercial potential and potential benefits of any product candidates of the combined company; that the proposed merger will close and will enable the combined company to participate in the possible success of the combined company’s product candidates; 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 Anchiano’s and Chemomab’s current expectations. Forward-looking statements involve risks and uncertainties.Because such statements deal with future events and are based on Anchiano’s and Chemomab’s current expectations, they are subject to various risks and uncertainties and actual results, performance or achievements of Anchiano or the combined company could differ materially from those described in or implied by the statements in this presentation, including: the risk related to Anchiano’s and Chemomab’s ability to complete the merger on the proposed terms and schedule, including risks and uncertainties related to the satisfaction of the closing conditions related to the merger agreement and risks and uncertainties related to the failure to timely or at all obtain shareholder approval for the transaction; the execution of definitive agreements with certain existing Chemomab shareholders including risks and uncertainties related to the satisfaction of the closing conditions related to the financing; the uncertain and time- consuming regulatory approval process; risks related to the combined company’s ability to correctly manage its operating expenses and its expenses; risks related to the market price of Anchiano’s ADSs relative to the exchange ratio; unexpected costs, charges or expenses resulting from the transaction; potential adverse reactions or changes to business relationships resulting from the announcement or completion of the proposed merger transaction; combined company’s plans to develop and commercialize its product candidates, including CM-101 and RAS; the timing of initiation of combined company’s planned clinical trials; the timing of the availability of data from combined company’s clinical trials; the timing of any planned investigational new drug application or new drug application; combined company’s plans to research, develop and commercialize its current and future product candidates; the clinical utility, potential benefits and market acceptance of combined company’s product candidates; combined company’s commercialization, marketing and manufacturing capabilities and strategy; the combined company’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 favorable terms or at all. In addition, there can be no assurance that Anchiano and Chemomab will be able to complete the transactions contemplated by the merger agreement or related transactions. Additional risks and uncertainties relating to Anchiano and its business can be found under the caption “Risk Factors” and elsewhere in Anchiano’s filings and reports with the SEC, including in the Company’s Annual Report on Form 10-K for the year ended December 31, 2019 filed with the SEC on March 17, 2020 as updated by its Quarterly Reports on Form 10-Q for the quarters ended March 31, 2020, June 30, 2020 and September 30, 2020, filed with the SEC on May 7, 2020, August 14, 2020 and November 16, 2020, respectively, and its other subsequent filings with the SEC. Anchiano expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in Anchiano’s and Chemomab’s expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.This presentation (“Presentation”) is for informational purposes only and does not constitute an offer to sell, solicitation of an offer to buy, or a recommendation to purchase any equity, debt or other financial instruments of Anchiano Therapeutics Ltd. (“Anchiano”) or Chemomab Ltd. (“Chemomab”) or any of Chemomab or Anchiano’s affiliate securities (as such term is defined under the U.S. federal securities laws). The information contained herein does not purport to be all-inclusive and is qualified in its entirety by the definitive merger agreement entered in December 14, 2020 filed by Anchiano on a Current Report on Form 8-K on December 15, 2020. The data contained herein is derived from various internal and external sources. No representation is made as to the reasonableness of the assumptions made within or the accuracy or completeness of any other information contained herein. All levels, prices and spreads are historical and do not represent current market levels, prices or spreads, some or all of which may have changed since the issuance of this document. Any data on past performance, modeling contained herein is not an indication as to future performance. Anchiano and Chemomab assume no obligation to update the information in this Presentation. Neither Anchiano or Chemomab accepts any liability whatsoever for any losses arising from the use of this Presentation or reliance on the information contained herein. Nothing herein shall be deemed to constitute investment, legal, tax, financial, accounting or other advice. This Presentation is being provided for use only by the intended recipient. No representation or warranty (whether expressed or implied) has been made by Anchiano, Chemomab or any of their respective affiliates with respect to the matters set forth in this Presentation, and the recipient disclaims any such representation or warranty. Only those particular representations and warranties of Anchiano, Chemomab or any of their respective affiliates made in a definite written subscription agreement, if any, regarding the matters set forth in this Presentation (which will not contain any representation or warranty relating to this Presentation or information contained in or omitted from this Presentation) when and if executed, and subject to such limitations and restrictions as specified therein, shall have any legal effect. At any time upon the request of Anchiano for any reason, recipient shall promptly deliver to Anchiano or securely destroy this Presentation and any other documents furnished to recipient by or on behalf of Anchiano or Chemomab without keeping any copies, in whole or part, thereof.Non-Confidential2

Chemomab Highlights A Clinical Stage Biotech CompanyFocus • Development of innovative therapies for multiple fibrotic diseasesClinical Differentiation• CM-101, a first-in-class CCL24 neutralizing mAb with confirmed anti-fibrotic MoA • Validated CCL24 as critical fibrosis target: clinical findings and experimental models • Positive Ph1b data including safety, tolerability, PK, PD and biomarker readoutsNear-Term Catalysts• Initiating staggered phase 2 clinical programs, with first started in 4Q20 • Clinical readouts are expected over the next 12-18 months to drive value inflectionRobust IP Portfolio• Issued CoM, multiple nationalization stage filings, worldwide patent exclusivity through 2041Top Tier InvestorsCoM- Composition of matter 3

Experienced LeadershipManagementADI MOR, PhD Chief Executive Officer, Co-FounderARNON AHARON, MD Chief Medical OfficerSIGAL FATTAL, CPA Chief Financial OfficerSHARON ELKOBI, MSc, MBA VP Business DevelopmentMICHAL SEGAL-SALTO, PhD VP Research and DevelopmentSHARON HASHMUELI, PhD Head of CMC and Regulatory AffairsBoard of Directors Scientific Advisory BoardSTEPHEN SQUINTO, PhD Chairman of the BoardNISSIM DARVISH, MD, PhD DirectorJASON CAMM DirectorADI MOR, PhD Chief Executive Officer & Co-FounderDAVID BEN AMI DirectorProf. Marco Matucci, Cerinic, MD, PhD Director of the Division of Rheumatology, University of Florence, ItalyProf. Dinesh Khanna MD, MBBS, MSc Director of the Scleroderma Program, University of Michigan, Ann Arbor, Michigan, USAProf. Francesco Del Galdo, MD, PhD Head of the Scleroderma Program at NIHR, University of Leeds, UKScott L. Friedman, MD The Dean for Therapeutic Discovery and Chief, Division of Liver Diseases, Mount Sinai, NY, USAMassimo Pinzani, MD, PhD, FRCP Sheila Sherlock Chair of Hepatology, Director UCL Institute for Liver and Digestive Health, RFH, London, UKGideon Hirschfield, MA MB PhD Lily and Terry Horner Chair in Autoimmune Liver Disease, University of Toronto, Toronto General Hospital, Canada4

Chemomab Strategy: Fibrotic Disease Franchise Addressing Fibrotic Diseases with High Unmet NeedINDICATIONCANDIDATEDISCOVERY PRECLINICALPHASE 1 PHASE 2 PIVOTALPRIMARY SCLEROSING CHOLANGITHISSYSTEMIC SCLEROSISCM-101 (IV) CM-101 (IV)Orphan designation granted from FDA and EMA Orphan designation granted from FDA and EMAANTI FIBROTIC MoA in LIVER FIBROSISCM-101 (SC)Long term evaluation of SC formulation, Biomarkers selectionNEXT GENERATION-BI SPECIFIC TARGETINGFIBROSISSCREENINGCombination target screeningIV- Intravenous SC- Subcutaneous TBD- To be determined 5

Fibrotic Diseases – Unmet Medical Need Potentiating High Morbidity and MortalityFibrotic DiseaseOrphan DiseaseSOCSequelaMedian Survival7MM Prevalence ValuePrimary Sclerosing Cholangitis (PSC)Systemic Sclerosis (SSc)Symptomatic approach, UDCA (EU), Liver Transplant - the only disease modifying optionSymptomatic approach, Nintedanib approved for ILD. No disease modifying optionBile duct damage, liver fibrosis, cirrhosis, cholangiocarcinomaSkin fibrosis, vasculopathy multi-organ failure (lung, GI, heart)10 – 12 yr10 yr70K pts140K pts>1B$>1B$No disease-modifying drugs have been approved for these fibrotic disorders7MM- 7 major markets; US, 5EU and JapanNon-ConfidentialILD– Interstitial Lund Disease 6

CCL24 is a Novel Therapeutic Target for Fibrosis Critical Mediator Promoting Inflammation and FibrosisCCL24-secreting cells M2 Macrophages, Immune and Epithelial cellsCCL24CCL24-regulated cells Fibroblasts-Liver, Lung and skin, Immune cells, and Cholangiocyte Dual role in promoting fibrosis - directly activates fibroblasts - enhances local immune cell recruitmentCCR3 Unique and differentiated activity- ex vivo and in vivo data confirms unique role vs other CCLs- correlates with disease outcome and fibrotic biomarkersImmune cells recruitment Fibroblasts activationTissue scarring, inflammatory-mediated damage, collagen deposition Minor expression in healthy tissue - significantly elevated in liver, skin, lung fibrotic tissue - wide therapeutic margin Positive feedback loop potentiates tissue damage - responsible for initiation and perpetuation of fibrosisDamaged tissue CCL24 SecretionOrgan failure7

CCL24: a Critical Node Potentiating Fibrosis-Related Diseases Target Validation in PSC and SScCCL24 level in SSc patients’ skinCCL24 level in SSc patients’ serumCCL24 serum level in PSC patients correlates with ELF fibrotic biomarkerCCL24 level in PSC patients’ liverGreen-CCL24; Red-CD31Collaboration with University of FlorenceCollaboration with Royal Free (UK)• CCL24 expression are significantly and selectively elevated in diseased vs. healthy tissues• CCL24 levels correlates with disease progression and circulating fibrotic biomarkers• CCL24 functionally drives critical fibrotic pathways across several experimental models• CCL24 blockade using CM-101 demonstrates first evidence of anti-fibrotic activity in humanELF – Enhanced Liver Fibrosis ALP – Alkaline Phosphatase 8

CCL24 Blockade is Singularly Sufficient to Attenuate Fibrosis Knocking out the CCL24 gene attenuates bleomycin Induced (SSc) model1.81.6Dermal thickness*Immune cell lung infiltration50001.41.210.84000300020001000*0.6WT PBS WT BLM CCL24 KO- PBSCCL24 KO- BLM0 WT-BLM CCL24 KO-BLMCCL24 KO-BLMCCL24 KO-PBSα SMA expression in skin lesions 65 * 43210 WT- PBSWT- BLMCCL24 KO- PBSCCL24 KO- BLMWT-BLMWT-PBSNon-Confidential*p ≤0.05BLM - Bleomycin WT - Wild type KO - Knock out9

CM-101- A First in Class mAb Blocking CCL24 Dual Mechanism of Action Interfering with the Core Fibrotic Pathways CM-101 Fully humanized antibody, binds and blocks CCL24 withCCR3CCL24high affinity CM-101’s epitope directly interfering with Receptor-InflammationImmune cells recruitmentFibrosisFibroblasts activation & proliferationLigand interaction Significant attenuation of fibrosis across several liver, skin and lung fibrosis models Favorable PK profile (IgG1) Two formulations: IV and SC• Well defined manufacturing process Strong IP portfolio based on issued CoM patentsNon-ConfidentialCoM - Composition of Matter 10

CM-101 Reduces Liver Fibrosis by 80% Reduced Liver Collagen in TAA Liver Fibrosis Rat Model Using Therapeutic DesignSIRIUS RED (COLLAGEN)10080604020082% reductionTAA TAA +CM-101 (2.5mg/kg)Pro-fibrotic genesLiver enzymesCol1A1 Col3A1 TIMP1 ACTA2 TGF-βALT AST ALPSegal-Salto et al, JHEP reports 2020Non-ConfidentialTAA- Thioacetamide 11

CM-101 Profoundly Reduces Skin and Lung Fibrosis in SSc Skin and Lung Experimental Models Relevant to Systemic Sclerosis Using Therapeutic DesignBleomycin (SC) induced dermal fibrosis100Normalizes skin and lung fibrosis levels in bleomycin induced models using therapeutic dosing after disease evident** 80 * * 604020Demonstrates a dose dependent0 Vehicle BLM BLM+ CM-101 0.5mg/kgBLM+ CM-101 1mg/kgBLM+ CM-101 2.5mg/kgBLM+ lgGattenuation of fibrosisSubstantially reduces lung collagen and inflammation as compared to approved drugs for lung fibrosisBleomycin (IT) induced lung fibrosisMor et al, Annals of Rheumatoid Diseases, 2019**p ≤0.01; *p ≤0.05.BLM, bleomycin. IT, Intratracheal 12 SC, Subcutaneous12

CM-101 Holds a Robust Preclinical Package Significantly Attenuates Fibrosis & Inflammation Across a Wide Range of ModelsCCL24 Target ValidationEx-Vivo (Patient Samples) PSC • Biomarkers correlation • Overexpression of CCL24 and CCR3 Systemic Sclerosis • Fibrotic biomarkers correlation • Disease deterioration correlation • Overexpression of CCL24 and CCR3 NASH • Disease severity correlation • Overexpression of CCL24 and CCR3 In-Vivo (Knockout Animal Models) Systemic Sclerosis• CCL24 knock out vs. WT in Bleomycin induced skin fibrosis model (mice) NASH • CCL24 knock out vs. WT in MCD induced NASH (mice)Proof of Concept Animal ModelsPrimary sclerosing cholangitis • ANIT induced cholestasis-chronic and acute (mice) • Bile duct ligation (rat) • MDR2 knock-out (mice)Systemic sclerosis • Bleomycin-induced skin fibrosis (mice) • Bleomycin induced lung fibrosis (mice)Liver Fibrosis • TAA induced liver fibrosis (rat and mice)Nonalcoholic steatohepatitis • STAM (mice) • MCD diet induced NASH (mice)Atherosclerosis • ApoE knock out model (mice)Mechanism of Action CM-101 effects on fibroblasts activation • Dermal, Hepatic and Lung fibroblast activation• Dermal and liver fibroblast transition to myofibroblasts • Hepatic fibroblast motilityCM-101 effects on immune cells migration and recruitment • Dermal fibroblast migration • Monocyte polarization • Monocytes recruitmentToxicology• Short-term GLP in rodents • Long-term GLP in Non-human primates • Ex-vivo safety: ADCC, CDC, cytokine secretion • Tissue cross reactivityNon-Confidential13

CM-101 is Safe & Well Tolerated in Healthy Volunteers Phase 1a Single Administration study• CM-101 was safe and well tolerated at all tested doses up to 10 mg/kg and for both formulations• Average t1/2 of 19-21 days (for IV and SC), supports long interval administration once every 2-4 weeks• Dose dependent target engagement measured by serum CCL24 levelsIV Phase 1SC Phase 1Double-Blind, Randomized Escalating Dose (N=32)CM-101 0.75 mg/kg IV or placebo Follow-up period (6 weeks)CM-101 2.5 mg/kg IV or placeboCM-101 5 mg/kg IV or placeboCM-101 10 mg/kg IV or placeboEnd of 42 days follow-up periodDouble-Blind, Randomized Single Dose (N=8) CM-101 5 mg/kg SC or placebo• Comparable target engagement & PK Profiles for the SC and IV formulationsScreening period (up to 28 days)n=40 healthy volunteersEnd of 42 days follow-up periodNon-ConfidentialIV - Intravenous SC - Subcutaneous 14

Ph1b Demonstrates Safety & Tolerability Along 15 Weeks Treatment Phase 1b Multiple Administration Study in NAFLD Patients• Study population- NAFLD patients with normal liver functionDouble-Blind, Randomized Escalating Dose (N=16)• Multiple CM-101 administrations were safe and well tolerated using both IV and SC formulationsPhase 1bCM-101 2.5 mg/kg IV or placebo• Favorable t1/2, supports long dosing interval (Q2W - Q4W)Day 0CM-101 5 mg/kg SC or placeboWk 15Wk 18• Dose dependent PK and target engagementRandomizationEnd of treatmentEnd of study• Tested doses - 2.5 mg/kg IV infusion and 5 mg/kg SC injection • 5 repeated administrations per patient; Q3W • Primary endpoint - safety and tolerabilityIV - Intravenous SC - Subcutaneous Wk - week 15

CM-101 Target Engagement & Anti-Fibrotic Mechanism Human Confirmation for CM-101 Anti-Fibrotic Mechanism of ActionPK-PDFibrotic Biomarkers* & ElastographyPK-PD 2.5mg/kg IV 2520151050 0 21 42 63 84 105 126CCL24 (Target Eng.) CM-101150100 10 2050 10 00 0CM-101 Placebo30150Time (days) 60 PK-PD 5mg/kg SC40EOT250200150100-10-20ProC4-10-20TIMP1-15-30FibroScan™20 Nordic Biosciences , Denmark 500 0 0 21 42 63 84 105 126*Concordant results across 6 relevant fibrotic markersTime (days)EOTProC4-Procollagen 4 TIMP1- metallopeptidase inhibitor 1 16 EOT-End of Treatment16

CM-101 Clinical Development Plan and Key Catalysts Phase 2 Studies Driving Pivotal Studies2020 2021 2022Primary Sclerosing Cholangitis (IV formulation)Phase 2: 12 wk treatment *Randomized placebo-controlled; Europe and Israel study sitesFPI Q4/20IA LPI Q4/21POCSystemic Sclerosis (IV formulation)Phase 2: 24 wk treatment Randomized placebo-controlled; US, Europe study sitesLiver Fibrosis Proof of MoA (SC formulation)FPIPhase 2a: 14 wk treatment Randomized placebo-controlled; Israel study sitesLPIPOCFPIPOCFPI: First patient in, LPI: Last patient in, IA: Interim assessment POC: Proof of Concept, IV: Intravenous, SC: Subcutaneous *NCT04595825 17

Chemomab, Fighting Fibrosis Across IndicationsOpportunity Clinical stage company entering Ph2 trials in multiple fibrotic indications with high unmet need Substantial value inflection points in 2021-2022 Strong leadership with proven track recordCM-101 First-in-class mAb blocking CCL24 Novel and differentiated dual anti-fibrotic and anti- inflammatory MoA SC and IV Formulation Strong IP protectionEfficacy First anti-fibrotic evidence in patients Significant anti-fibrotic effects across multiple in vivo, ex vivo and in vitro modelsSafety Favorable safety and tolerability that support chronic treatment based on toxicology, Phase Ia and Phase Ib clinical trialsPK & Mode of Administration Optimal PK for both SC and IV formulations Comparable Exposure levels and target engagement using both formulationsIV - Intravenous SC - Subcutaneous 18

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