—New Clinical and Translational Data Presented at Major Medical Meetings Further Confirms the Disease-Modifying Potential of Nebokitug in Primary Sclerosing Cholangitis and Suggests Possible Additional Benefit in PSC Patients with Co-Existing IBD—
—Company Continues to Advance Multiple Partnering Options for Nebokitug—
“In the first quarter we continued to have productive discussions with potential strategic partners while releasing new data analyses that further extend our understanding of the therapeutic potential of nebokitug and its CCL24 target,” said
First Quarter 2026 and Recent Highlights:
- On
May 30, 2026 , Chemomab will present data from three abstracts at EASL 2026, the Annual Congress of theEuropean Association for the Study of the Liver inBarcelona, Spain .
- 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.
- In one EASL 2026 study1,
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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.
- 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.
- 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
- 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) inChicago, USA 4. Dr.Parvez Mantry ofMethodist 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.
1 - AI-driven proteomic profiling differentiates composite improvement following treatment with nebokitug in PSC;
2 - Nebokitug down-regulates core fibrotic and immune pathways defined by single-cell liver profiling; R Aricha, T Snir, J Lawler, C Cirillo, D Weiner, A Mor; EASL 2026 Abstract No. 1852; Immune-mediated and cholestatic disease: Clinical aspects;
3 - Nebokitug modulates gut-liver inflammatory and tissue remodeling signatures in PSC patients with coexisting IBD; R Aricha, T Snir, J Lawler, C Cirillo, D Weiner, and A Mor; EASL 2026 Abstract No. 1859; Immune-mediated and cholestatic disease: Clinical aspects;
4 - Nebokitug modulates inflammatory and tissue-remodeling signatures in patients With PSC and coexisting IBD: Biomarker findings From the SPRING Phase 2 trial;
First Quarter 2026 Financial Highlights
- Cash Position: Cash, cash equivalents and short-term bank deposits were
$8.0 million as ofMarch 31, 2026 , compared to$10.4 million as ofDecember 31, 2025 . This cash runway is expected to fund the company through the end of the first quarter of 2027.
- 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 .
- 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.
- 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).
- 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.
- 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 ofDecember 31, 2025 .
Forward-Looking Statements
This press release contains forward-looking statements within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties. All statements other than statements of historical facts contained in this press release, including statements regarding our future financial condition, results of operations, business strategy and plans, and objectives of management for future operations, as well as statements regarding industry trends, are forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as “estimate,” “intend,” “may,” “plan,” “potentially,” “will” or the negative of these terms or other similar expressions. We have based these forward-looking statements largely on our current expectations and projections about future events and trends that we believe may affect our financial condition, results of operations, business strategy and financial needs. These forward-looking statements are subject to a number of risks, uncertainties and assumptions, including, among other things: the risk that certain acknowledgements from the End-of-Phase 2 (EOP2) meeting with the FDA in connection with PSC regulatory approval will not materialize into a pathway for regulatory approval; that certain conclusions and assumptions drawn from the EOP2 meeting with the FDA discussed in the Company’s press releases will prove incorrect and adversely affect the ability for nebokitug to become an FDA fully approved therapy; the risk that the full data set from the nebokitug study or data generated in further clinical trials of nebokitug will not be consistent with the topline results of the nebokitug Phase 2 PSC trial; failure to obtain, or delays in obtaining, regulatory approvals for nebokitug in the
About
Chemomab is a clinical stage biotechnology company developing innovative therapeutics for fibro-inflammatory diseases with high unmet need. Based on the unique role of the soluble protein CCL24 in promoting fibrosis and inflammation, Chemomab developed nebokitug, a first-in-class dual activity monoclonal antibody that neutralizes CCL24 and has demonstrated disease-modifying potential. In clinical and preclinical studies, nebokitug has been shown to have a favorable safety profile and has been generally well-tolerated, with the potential to treat multiple severe and life-threatening fibro-inflammatory diseases. Chemomab has reported positive results from five clinical trials of nebokitug. Based on positive data from its Phase 2 SPRING trial in primary sclerosing cholangitis (PSC), Chemomab and the FDA have aligned on the design of a nebokitug Phase 3 registration trial in patients with PSC. Nebokitug has received FDA and EMA Orphan Drug and FDA Fast Track designations for the treatment of PSC. Chemomab’s nebokitug program for the treatment of systemic sclerosis has received FDA and EMA Orphan Drug designations and has an open
Contacts:
Media & Investors:
Consulting Vice President
Investor & Public Relations,
Phone: +1 917-355-9234
barbara.lindheim@chemomab.com
| Interim Condensed Consolidated Balance Sheets (Unaudited) | ||||||
| In USD thousands (except for share amounts) | ||||||
| 2026 | 2025 | |||||
| Assets | ||||||
| Current assets | ||||||
| Cash and cash equivalents | 5,906 | 7,564 | ||||
| Short term bank deposits | 2,137 | 2,802 | ||||
| Other receivables and prepaid expenses | 3,431 | 3,059 | ||||
| Total current assets | 11,474 | 13,425 | ||||
| Non-current assets | ||||||
| Long term prepaid expenses | 167 | 211 | ||||
| Property and equipment, net | 167 | 176 | ||||
| Total non-current assets | 334 | 387 | ||||
| Total assets | 11,808 | 13,812 | ||||
| Current liabilities | ||||||
| Trade payables | 204 | 485 | ||||
| Accrued expenses | 296 | 337 | ||||
| Employee and related expenses | 613 | 656 | ||||
| Total current liabilities | 1,113 | 1,478 | ||||
| Total liabilities | 1,113 | 1,478 | ||||
| Shareholders' equity (*) | ||||||
| Ordinary shares no par value - Authorized: 4,650,000,000 shares as of Issued and outstanding: 576,030,200 Ordinary shares as of | - | - | ||||
| Additional paid in capital | 124,086 | 123,952 | ||||
| Accumulated deficit | (113,391 | ) | (111,618 | ) | ||
| Total shareholders’ equity | 10,695 | 12,334 | ||||
| Total liabilities and shareholders’ equity | 11,808 | 13,812 | ||||
(*) 1 American Depositary Share (ADS) represents 80 Ordinary Shares.
| Interim Condensed Consolidated Statements of Operations (Unaudited) | ||||
| In USD thousands (except for share and per share amounts) | ||||
| Three months | Three months | |||
| Ended | Ended | |||
| 2026 | 2025 | |||
| Operating expenses | ||||
| Research and development | 925 | 2,493 | ||
| General and administrative | 925 | 994 | ||
| Total operating expenses | 1,850 | 3,487 | ||
| Financing income, net | 77 | 164 | ||
| Loss before taxes | 1,773 | 3,323 | ||
| Taxes on income | - | - | ||
| Net loss for the period | 1,773 | 3,323 | ||
| Basic and diluted loss per Ordinary Share (*) | 0.003 | 0.007 | ||
| Weighted average number of Ordinary Shares outstanding, basic, and diluted (*) | 638,293,363 | 456,149,916 | ||
(*) 1 American Depositary Share (ADS) represents 80 Ordinary Shares
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