Acrivon Advances ACR-7280, an Optimized, AP3-Enabled, Potential First-in-Class, Oral CDK11 Inhibitor Toward IND Filing in First Half of 2027
Key Highlights
- ➤ACR-7280 showed complete tumor regression in aggressive AML xenograft models
- ➤IND-enabling studies underway; FDA submission remains on track for first half of 2027
- ➤ACR-7280 demonstrated synergy with venetoclax and menin inhibitors across AML models
- ➤Initial development will target AML as monotherapy and in combination
- ➤ACR-7280 was selected from multiple CDK11 inhibitor candidates for potent single-agent activity
Expert Statements
Peter Blume-Jensen, Chief executive officer, president and co-founder of Acrivon Therapeutics
“ACR-7280 provides another powerful validation of our AP3 innovation engine”
Peter Blume-Jensen, Chief executive officer, president and co-founder of Acrivon Therapeutics
“AP3 profiling and analyses enabled us to identify ACR-7280 as a highly selective CDK11 inhibitor with optimized, desirable cellular pathway effects, which has translated to complete tumor regression in aggressive AML mouse models.”
Peter Blume-Jensen, Chief executive officer, president and co-founder of Acrivon Therapeutics
“While CDK11 has historically been a difficult target to drug, we believe ACR-7280 provides a first-in-class opportunity with broad potential in refractory/relapsed AML.”
Peter Blume-Jensen, Chief executive officer, president and co-founder of Acrivon Therapeutics
“The oral administration route may also provide flexibility for combining with standard-of-care agents, like venetoclax and menin inhibitors, potentially in earlier line settings.”
Peter Blume-Jensen, Chief executive officer, president and co-founder of Acrivon Therapeutics
“We look forward to advancing ACR-7280 swiftly towards the clinic, with IND submission on track for the first half of 2027.”
ACR-7280 demonstrated complete tumor regression in aggressive AML xenograft models
Prioritized among multiple AP3-discovered, highly selective CDK11 inhibitor candidates based on potent single agent activity and strong synergy with BCL-2 and menin inhibitors
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