エドガーで原本を確認する
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Exhibit
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Description
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CHEMOMAB THERAPEUTICS LTD.
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Date: May 14, 2026
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By:
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/s/ Sigal Fattal
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Sigal Fattal
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Chief Financial Officer
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On May 30, 2026, Chemomab will present data from three abstracts at EASL 2026, the Annual Congress of the European Association for the Study of the Liver in Barcelona,
Spain.
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In one EASL 2026 study1, Olink-generated analyses of circulating proteins in patient samples from the SPRING trial were used to generate an AI/machine
learning model to identify patients who showed a combined improvement in all three key fibrosis-related measures: ELF score, liver stiffness as measured by
FibroScan© and PRO-C3. The model showed strong performance and reliability, accurately distinguishing patients who met the combined improvement definition from those who did not. The proteins driving this distinction were
primarily related to liver biology, including metabolism, protein breakdown, and extracellular matrix and tissue remodeling. The authors conclude that AI-generated proteomic analysis was successful in distinguishing a composite efficacy
improvement outcome in nebokitug-treated patients with PSC. Patients who met the criteria showed differential expressions of liver proteins, with functional liver
related proteins as the main drivers of this change. This analysis highlights the breadth of treatment-associated improvements following CCL24-blocking therapy with nebokitug, as well as the important role of CCL24 blockade in PSC
and other liver disease pathology.
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A second EASL 2026 study2 examined the impact of nebokitug treatment on four PSC-specific gene expression programs (GEPs) in patients with PSC. GEPs are the
coordinated patterns of gene activity that determine which genes are turned on or off, when, and to what extent, ultimately controlling cellular functions and phenotypes in the individual. The four GEPs, which researchers had previously
identified using single-cell analyses of human liver tissue, are upregulated in livers from patients with PSC compared to healthy controls or to patients with other liver disease. They include pathways associated with extracellular matrix
remodeling, macrophage activation, fibrosis/myofibrosis, and immune activation. The new analysis assessed the effects of treatment with nebokitug on these GEPs by examining protein changes in patient serum samples from the nebokitug SPRING
trial. Proteins corresponding to all four PSC-related GEPs, reflecting fibrosis-related collagens, fibrotic macrophage activity, myofibroblast pathways, and immune-activation signaling, were statistically significantly elevated in the SPRING
trial patients with moderate-advanced disease compared to those with mild PSC. Treatment with nebokitug was associated with statistically significant and dose-dependent reductions in the signatures linked to these PSC-related fibrotic and
immune proteins. These findings provide further support for nebokitug’s CCL24 blocking activity as a mechanism-based therapeutic approach targeting core molecular drivers of PSC pathogenesis.
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A third EASL 2026 study3 examined nebokitug and its CCL24 target in the context of the co-morbidity of PSC and inflammatory bowel disease (IBD). This
co-morbidity, which affects about 60-70% of all PSC patients, is thought to reflect their intertwined gut–liver immune pathways. In the nebokitug SPRING trial, 62% of enrolled PSC patients had concomitant ulcerative colitis (UC) or Crohn’s
disease (CD). This study evaluated whether CCL24 inhibition modulates inflammatory and tissue-remodeling signatures relevant to PSC-IBD pathogenesis. Serum proteins from SPRING trial patients were quantified using the Olink proteomic
platform. Biomarker analyses focused on inflammatory cytokines, chemokines, monocyte/macrophage markers, epithelial injury markers, and tissue-remodeling proteins previously associated with UC and CD activity. Nebokitug treatment led to modulation of inflammatory pathways shared between PSC and IBD in patients with moderate-advanced PSC. Significant reductions were observed in multiple
cytokines known to be strongly linked to IBD activation, mucosal immune recruitment and epithelial injury. Nebokitug also decreased multiple proteins associated with stromal and epithelial remodeling in IBD progression and demonstrated a
significant elevation in MST-1, a negative regulator of inflammation that has been linked to genetic susceptibility and disease modulation in IBD, highlighting its potential relevance to intestinal inflammatory pathways. The authors conclude
that treatment with nebokitug resulted in improvements across inflammatory and tissue-remodeling proteins relevant to PSC with coexisting intestinal inflammation from UC and CD. These findings suggest that CCL24 inhibition may beneficially
impact shared gut–liver inflammatory circuits in patients with co-existing PSC and IBD.
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On May 4, 2026, new data from the company’s Phase 2 SPRING trial of nebokitug in PSC was presented at Digestive Disease Week® (DDW 2026) in Chicago, USA4.
Dr. Parvez Mantry of Methodist Health System gave an oral presentation on a new proteomic study showing that treatment with nebokitug resulted in dose-dependent reductions in multiple inflammatory and tissue-remodeling signatures associated
with intestinal and hepatic immune activation. These proteomic changes are relevant to both primary sclerosing cholangitis (PSC) and inflammatory bowel disease (IBD), a debilitating chronic condition that affects about 60-70% of all patients
with PSC. In nebokitug-treated patients, especially those with moderate-advanced PSC, reductions in IBD-related inflammatory innate immune activation and epithelial remodeling biomarkers were observed. These proteomic changes indicate
disease-relevant target engagement and are consistent with modulation of biological pathways relevant to both PSC and IBD. The authors conclude that inhibition of nebokitug’s CCL24 target may provide meaningful benefit in PSC patients with
concomitant IBD.
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Cash Position: Cash, cash equivalents and short-term bank
deposits were $8.0 million as of March 31, 2026, compared to $10.4 million as of December 31, 2025. This cash runway is expected to fund the company through the end of the first quarter of 2027.
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Research and Development (R&D) Expenses: R&D expenses
were $0.9 million for the first quarter of 2026, compared to $2.5 million for the first quarter of 2025. The decrease in R&D expenses in the first quarter of 2026 compared to the first quarter of 2025 primarily resulted from the continued
winding down of activities related to the Phase 2 SPRING trial .
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General and Administrative (G&A) Expenses: G&A expenses were $0.9 million for the first quarter of 2026, compared to $1.0
million for the first quarter of 2025.
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Net Loss: Net loss in the first quarter of 2026 was $1.8 million, or a net loss of less than $0.01 per basic and diluted ordinary share, compared to $3.3 million, or a net loss of less than $0.01 per basic and diluted
ordinary share, for the first quarter of 2025. The weighted average number of ordinary shares outstanding, basic and diluted, in the first quarter of 2026 was 638,293,363 (equal to approximately 7,978,667 ADSs).
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Liquidity and Capital Resources: Chemomab believes its existing
liquidity resources as of March 31, 2026 will enable it to fund its operations through the end of the first quarter of 2027.
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Number of Issued and Outstanding Shares: As of March 31, 2026, the company had 576,030,200 Ordinary shares issued and outstanding (equal to approximately 7,200,377 ADSs), compared to 575,381,320 (equal
to approximately 7,192,266 ADSs) as of December 31, 2025.
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March 31,
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December 31,
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2026
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2025
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Assets
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Current assets
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Cash and cash equivalents
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5,906
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7,564
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Short term bank deposits
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2,137
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2,802
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Other receivables and prepaid expenses
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3,431
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3,059
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Total current assets
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11,474
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13,425
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Non-current assets
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Long term prepaid expenses
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167
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211
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Property and equipment, net
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167
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176
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Total non-current assets
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334
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387
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Total assets
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11,808
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13,812
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Current liabilities
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Trade payables
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204
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485
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Accrued expenses
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296
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337
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Employee and related expenses
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613
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656
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Total current liabilities
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1,113
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1,478
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Total liabilities
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1,113
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1,478
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Shareholders' equity (*)
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Ordinary shares no par value - Authorized: 4,650,000,000 shares as of March 31, 2026, and as of December 31, 2025;
Issued and outstanding: 576,030,200 Ordinary shares as of March 31, 2026 and 575,381,320 as of December 31, 2025;
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-
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-
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Additional paid in capital
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124,086
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123,952
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Accumulated deficit
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(113,391
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(111,618
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Total shareholders’ equity
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10,695
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12,334
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Total liabilities and shareholders’ equity
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11,808
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13,812
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Three months
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Three months
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Ended
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Ended
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March 31,
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March 31,
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2026
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2025
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Operating expenses
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Research and development
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925
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2,493
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General and administrative
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925
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994
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Total operating expenses
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1,850
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3,487
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Financing income, net
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77
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164
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Loss before taxes
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1,773
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3,323
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Taxes on income
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-
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-
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Net loss for the period
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1,773
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3,323
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Basic and diluted loss per Ordinary Share (*)
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0.003
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0.007
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Weighted average number of Ordinary Shares outstanding, basic, and diluted (*)
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638,293,363
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456,149,916
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