Cidara Therapeutics, Inc. (Nasdaq: CDTX) announced the company will deliver four poster presentations, including one late-breaking poster presentation, at this year’s American Association for Cancer Research (AACR) Annual Meeting being held April 5-10, 2024 at the San Diego Convention Center in San Diego, California.
- Multispecific CD73/PD-1 DFC demonstrates improved tumor reduction compared to PD-1 monotherapy in nonclinical study
- CCR5-targeting DFC demonstrates potent efficacy in colorectal cancer mouse model
- Late-breaking CBO421 data demonstrates improved efficacy compared to oleclumab in human triple-negative breast cancer cell lines
SAN DIEGO, April 05, 2024 (GLOBE NEWSWIRE) -- Cidara Therapeutics Inc. (Nasdaq: CDTX), a biotechnology company using its proprietary Cloudbreak® platform to develop drug-Fc conjugate (DFC) immunotherapies designed to save lives and improve the standard of care for patients facing serious diseases, announced the company will deliver four poster presentations, including one late-breaking poster presentation, at this year’s American Association for Cancer Research (AACR) Annual Meeting being held April 5-10, 2024 at the San Diego Convention Center in San Diego, California. The presentations highlight data on the company’s multispecific CD73/PD-1 drug Fc-conjugate (DFC), its CCR5-targeting DFC, and CBO421, its lead oncology DFC candidate targeting CD73.
“The preclinical data highlighted in our presentations at this year’s AACR meeting show the promise of our first-in-class or best-in-class DFCs to potentially improve treatment for a variety of cancers,” said Jeffrey Stein, Ph.D., president and chief executive officer at Cidara. “Our Cloudbreak platform has quickly produced DFC candidates effective in preclinical studies across various cancers with specific disease targets. This week, we are sharing data on our CCR5 DFC program for the first time, which has demonstrated robust efficacy as a monotherapy in mouse models of colorectal cancer. Targeting CCR5 has the potential to improve response rates to immune checkpoint inhibitor therapies, which could have a greater impact for patients unresponsive to these current treatment options. Additionally, our multispecific CD73/PD-1-targeting DFC and CBO421, our lead CD73-targeting DFC, continue to demonstrate antitumor efficacy, and we look forward to further advancing these candidates toward the clinic.”
Presentation details are summarized below:
Abstract Title: Discovery of a multispecific CD73/PD-1 targeting Drug Fc-Conjugate (DFC), which improves tumor reduction compared to PD-1 monotherapy in a humanized mouse model
Presenter: James Levin, Ph.D.
Date and Time: Monday, April 8, 2024, 1:30-5:00 PM PT
Key Highlights:
- First-in-class CD73/PD-1 targeting DFC is comprised of a multivalent conjugate of a small molecule CD73 inhibitor stably linked to a proprietary human IgG1 Fc-fusion with a PD-1 inhibitor peptide
- Multispecific DFC demonstrated potent inhibition of tumor growth in a humanized mouse model and was more potent than PD-1 monotherapy
Abstract Title: CBO421, a novel drug Fc-conjugate, inhibits the enzymatic activity of CD73 and triggers CD73 internalization
Presenters: Elizabeth Abelovski and Nicholas Dedeic
Date and Time: Monday, April 8, 2024, 9:00 AM-12:30 PM PT
Key Highlights:
- CD73 is a cell surface enzyme responsible for the production of adenosine, which is immunosuppressive and leads to immune evasion in solid tumors
- Adenosine production can be inhibited therapeutically by enzyme inhibition and receptor internalization and subsequent degradation
- In human triple-negative breast cancer cell lines, CBO421 demonstrated potent and complete CD73 enzyme inhibition and robust CD73 receptor internalization in CD73 cancer cells, superior to oleclumab, an anti-CD73 monoclonal antibody
Abstract Title: CBO421: A novel drug Fc-conjugate to prevent tumor immune evasion via the CD73/adenosine pathway
Presenters: Amanda Almaguer and Doug Zuill
Date and Time: Monday, April 8, 2024, 1:30-5:00 PM PT
Key Highlights:
- CBO421 demonstrated strong binding affinity and potent inhibition of both soluble and membrane bound CD73, differentiating it from monoclonal antibody CD73 inhibitors
- The candidate also exhibited high potency in functional cell-based assays and robust antitumor efficacy in a syngeneic mouse model
Abstract Title: CCR5-001, a novel Drug Fc-Conjugate (DFC) targeting CCR5, demonstrates potent efficacy in a colorectal cancer mouse model
Presenter: Simon Döhrmann, Ph.D.
Date and Time: Monday, April 8, 2024, 1:30-5:00 PM PT
Key Highlights:
- CCR5 is expressed on multiple immune cells and can contribute to an immune-suppressive tumor microenvironment, limiting response to immune checkpoint inhibitors
- First-in-class CCR5-targeting DFC, CCR5-001, demonstrated potent CCR5 binding and functional inhibition of CCR5 signaling in cell-based assays
- The candidate also demonstrated robust efficacy as a monotherapy in a syngeneic colorectal cancer mouse model, representing a potential to target CCR5 with DFCs in solid cancers where pathology is driven by the CCR5/CCL5 axis
About Cidara Therapeutics
Cidara Therapeutics is using its proprietary Cloudbreak® platform to develop novel drug-Fc conjugates (DFCs). These targeted immunotherapies offer the unique opportunity to create “single molecule cocktails” comprised of targeted small molecules and peptides coupled to a human antibody fragment (Fc). DFCs are designed to save lives and improve the standard of care for patients facing cancers and other serious diseases by inhibiting specific disease targets while simultaneously engaging the immune system. In addition, Cidara received FDA approval for REZZAYO™ (rezafungin for injection), which it has licensed to multiple partners to commercialize in the U.S. and ex-U.S. Cidara is headquartered in San Diego, California. For more information, please visit www.cidara.com.
Forward-Looking Statements
This release contains “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and such forward-looking statements are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. “Forward-looking statements” describe future expectations, plans, results, or strategies and are generally preceded by words such as “anticipates,” “believe,” “could,” “expect,” “may,” “plan” or “will”. Forward-looking statements in this release include, but are not limited to, statements related to whether nonclinical data generated for the multispecific CD73/PD-1 targeting DFC or any other conjugate will be predictive of activity in humans, whether a CCR% inhibitor DFC will have a benefit when combined with a checkpoint inhibitor therapy, and whether any oncology DFC will progress to further nonclinical or clinical development. Such statements are subject to a multitude of risks and uncertainties that could cause future circumstances, events, or results to differ materially from those projected in the forward-looking statements. These and other risks are identified under the caption “Risk Factors” in Cidara’s Annual Report on Form 10-K for the fiscal year ended December 31, 2022, and other filings subsequently made with the Securities and Exchange Commission. All forward-looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. Cidara does not undertake any obligation to publicly update any forward-looking statements, whether as a result of the receipt of new information, the occurrence of future events or otherwise.
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