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ACR-2316, which was internally discovered using biological SAR enabled by AP3 to overcome limitations of benchmark clinical WEE1 and PKMYT1 inhibitors, demonstrates potent anticancer activity in preclinical studies and is planned for monotherapy clinical development
AP3 profiling uncovered actionable pathways linked to resistance mechanisms for ACR-368, a clinical-stage CHK1/2 inhibitor, and identified ultra-low dose gemcitabine (ULDG) to sensitize resistant ovarian cancer cells to ACR-368
WATERTOWN, Mass., April 10, 2024 (GLOBE NEWSWIRE) -- Acrivon Therapeutics, Inc. ("Acrivon" or "Acrivon Therapeutics") (NASDAQ:ACRV), a clinical stage biopharmaceutical company developing precision oncology medicines that it matches to patients whose tumors are predicted to be sensitive to each specific medicine by utilizing its proprietary proteomics-based patient responder identification platform, Acrivon Predictive Precision Proteomics (AP3), today announced data from two posters that the company presented at the American Association for Cancer Research (AACR) Annual Meeting.
"Our data at AACR illustrate several of the broad capabilities of our AP3 platform and the power of employing this precision proteomics-based approach in both drug discovery and drug development," said Peter Blume-Jensen, M.D., Ph.D., chief executive officer, president, and founder of Acrivon Therapeutics. "Uniquely enabled by AP3, we designed a selective and potent dual inhibitor of both WEE1 and PKMYT1, ACR-2316, designed for potent single agent activity. We presented preclinical data showing its superior activity versus benchmark WEE1 and PKMYT1 single-agent inhibitors in multiple cancer models and look forward to advancing this compound into the clinic. Additionally at AACR, we presented data on the underlying mechanisms that drive resistance to treatment with ACR-368, which were discovered through AP3 profiling, and which led to the identification of ULDG as a way to sensitize resistant ovarian cancer cells to ACR-368. These actionable insights highlight Acrivon's differentiated approach to drug development."
In a poster titled "ACR-2316: A potentially first-in-class, potent, selective WEE1/PKMYT1 inhibitor rationally designed for superior single agent activity through synergistic disruption of cell cycle checkpoints," preclinical data showing that ACR-2316 is a potent dual WEE1/PKMYT1 inhibitor with superior anticancer activity were presented. ACR-2316 was highly potent across multiple human tumor cell lines and patient-derived ex vivo tumor models. In proliferation assays across a panel of 19 cancer cell lines, ACR-2316 demonstrated greater potency in all cell lines tested compared to adavosertib and lunresertib (mean IC50 = 70, 252 and 364 nM, respectively). In the 12 ovarian cancer patient-derived xenograft models tested, superior ex vivo anticancer activity of ACR-2316 was observed compared to azenosertib and lunresertib (mean IC50 = 9, 248 and 1620 nM, respectively). The complete responses observed with ACR-2316 in human tumor xenograft mouse models were associated with strong WEE1 and balanced PKMYT1 inhibition activity in tumors.
In the second poster titled "Acrivon predictive precision proteomics (AP3) uncovers mechanism of resistance to ACR-368, a clinical-stage CHK1/2 inhibitor, and identifies rational combination treatment," preclinical studies using five ovarian cancer cell lines that were generated to be durably resistant to ACR-368 were reported. These cell lines were profiled using AP3 mass spectrometry, and comprehensive pathway reconstitution, and kinase activity analysis was performed to identify drug resistance mechanisms to ACR-368 to uncover actionable vulnerabilities. As a result, ULDG was identified as a rational sensitization treatment, and in in vivo CDX and PDX models of ovarian cancer, data confirmed that ULDG sensitizes cancer cells to ACR-368. This corresponded with the subsequent upregulation of ACR-368 OncoSignature biomarkers, indicating that the OncoSignature assay can predict which ULDG sensitized tumors would be responsive to treatment with ACR-368.
Posted In: ACRV
