Chemomab Therapeutics Ltd. Q3 FY2022 earnings call

• Advanced clinical programs for CM-101, including progress on Phase II liver fibrosis biomarker data, opening new sites for Phase II PSC trial, and designing Phase II SSC trial.
• Unveiled promising clinical data from an investigator-initiated lung injury study showing CM-101 reduced biomarkers of lung inflammation and fibrogenesis in hospitalized COVID patients with severe pneumonia.
• Presented preclinical data at scientific meetings supporting CCL-24 role in PSC pathophysiology and using biomarkers in drug development.
• Updates on CM-101 liver fibrosis trial on track for year-end readout, PSC trial recruitment efforts, and details on SSC trial design including patient inclusion criteria and outcome measures.

Cash, cash equivalents and bank deposits were $46.5 million as of September 30, 2022 compared to $51.8 million at June 30, 2022. R&D expenses were $5.4 million for the quarter ended September 30, 2022 compared to $1.5 million for the same quarter in 2021. G&A expenses were $2.9 million for the quarter ended September 30, 2022 compared to $1.4 million for the same quarter in 2021. Net loss was $8.1 million or a net loss of approximately $0.035 per basic and diluted ordinary share for the third quarter of 2022 compared to $3 million or a net loss of approximately $0.013 per basic and diluted ordinary share for the quarter ended September 30, 2021. No detailed breakdown of product segments by revenue contribution is provided.

• Runway to last through end of 2023.
• Anticipate top line data from liver fibrosis biomarker trial by year-end.
• PSC trial on track to report top line data from double-blind portion in second half of 2024.
• SSC trial expected to be open for enrollment by end of 2023 or early Q1 2023, with top line data in second half of 2024.

Factors such as those affecting clinical trial outcomes, market conditions, and uncertainties in drug development processes as mentioned in the forward-looking statement, including risks that could cause actual results to materially differ from forward-looking statements.

Q: Hi, good morning. And good afternoon, everybody. Thanks for taking my question. First on SSC, could you talk about the percent of the overall patient population that has these higher levels of CCL-24 that you're hoping to enroll? And then I know that preclinically, you've shown a correlation to CCL-24 levels and disease severity. So should we be expecting these patients to be more on the moderate to severe disease spectrum?

A: David Weiner: Yes, we are actually mapping out currently what CCL-24 levels look like across the systemic sclerosis population. The intent in the trial is to not impair enrollment. So we'll enroll those probably with roughly about 70%, 75% tile or greater levels within systemic sclerosis as we screen. Adi Mor: Yes. Thank you. So I just can add to your second question, Kristen, and thank you for that, is that indeed, we have said in the past that CCL-24 correlate with several measurements and manifestations of systemic sclerosis, pulmonary, digital or vascular-related one as well as some fibrotic-related biomarkers like ELF. So we do see that - or believe that this population with the cut-off – it will be determined will provide a better chance for success in terms of enrolling the more relevant patients with CCL-24 and the ones that are more active overall in the different spaces.

Q: I guess two questions. One, I guess, just following on the biomarker discussion. Is there a way that you've looked at to evaluate if the CCL-24 elevation is a result of the inflammatory state or if it's a driver saying using related biomarkers, though as to differentiate those patient populations more discriminately as to who are likely to be responders to therapy? And then on the PSC side, I believe you indicated top line data from the blind port population or the blinded portion of the study in 2H 24. Have you given any thought to reporting our interim data perhaps on the original 10 mg per kg cohort? Thanks.

A: David Weiner: Yes, that is certainly a consideration we make – we have. That is an option that we can include, particularly since that cohort is likely as you surmise to enroll in the nearer term than the full - than all the additional cohorts that we added through the recent amendment and trial expansion. As we position the study and think about the study, it is our hope in the longer run that this could be a regulatorily supportive study. And as such, we would like to protect it in that sense. And so that decision, although it's an option to us is, those are the two things that we're weighing, an earlier look at data versus the [indiscernible] when you do an interim analysis on study power for any particular outcome. Adi Mor: Yeah, I think you covered that very well. You were asking, Jeff, if it's kind of the cause or part of the cycle. And for systemic sclerosis and PC we're obviously not familiar with what is the cause of disease, but we have seen preclinically, the CCL-24 is involved in kind of perpetuating this vicious cycle of inflammation and fibrosis. So even if the injury is some kind of an environmental or genetic kind of reason, CCL-24 was found by our models to kind of further progress the disease in this vicious cycle by its expression alone