Trial-by-gene · CDKN2A
Active trials enrolling CDKN2A loss / MTAP-deleted solid tumors
Decision-support aid only — eligibility decisions must be confirmed against the actual trial protocol and the patient's medical record. Trial counts and statuses change daily; this page is for orientation, not adjudication.
CDKN2A homozygous deletion frequently co-deletes MTAP (adjacent on 9p21), creating vulnerability to PRMT5 inhibitors and MAT2A inhibitors via synthetic lethality. CDK4/6 inhibitor sensitivity also follows from CDKN2A loss in select contexts. Active trials are mostly phase I/II first-in-human in MTAP-deleted solid tumors.
Browse the live listing
Search ClinicalTrials.gov for trials with CDKN2A loss-of-function or co-deleted MTAP loss as biomarker eligibility.
Open ClinicalTrials.gov listingSource: ClinicalTrials.gov, US National Library of Medicine. Trial-listing data is in the public domain. Use of ClinicalTrials.gov data must comply with the NLM terms of use.
Representative trial phases and designs
Phase I, MTAP-deleted
PRMT5 inhibitors (AMG 193, MRTX1719, others) in MTAP-deleted advanced solid tumors.
Phase II, CDK4/6
Abemaciclib or palbociclib in CDKN2A-altered or RB-intact solid tumors.
Eligibility notes
Most PRMT5/MAT2A inhibitor trials require homozygous MTAP deletion (typically confirmed by NGS or IHC). Heterozygous loss is generally insufficient.
Frequently asked questions
- Why does MTAP loss matter when the gene is CDKN2A?
- MTAP is adjacent to CDKN2A on chromosome 9p21. ~80% of CDKN2A homozygous deletions co-delete MTAP. MTAP loss creates the metabolic vulnerability that PRMT5 and MAT2A inhibitors exploit.