OnCo
targetsTarget

PRMT5 (MTAP-deleted cancers)

An enzyme that cancers lacking the MTAP gene (about 10-15% of all tumours) depend on more than normal cells do; new inhibitors designed to exploit that difference are in late trials.

Homozygous deletion of MTAP (co-deleted with CDKN2A on 9p21) causes accumulation of MTA, which partially inhibits PRMT5, leaving MTAP-null cells hypersensitive to further PRMT5 inhibition. MTA-cooperative PRMT5 inhibitors (AMG 193, MRTX1719/BMS-986504, TNG908, TNG462, AZD3470) exploit this synthetic lethality with a wide therapeutic window compared with first-generation PRMT5 inhibitors (which caused thrombocytopenia). Responses have been reported in MTAP-deleted NSCLC, mesothelioma, pancreatic and biliary cancers; combination with KRAS G12C inhibitors is being tested and phase 3 trials began in 2025-26. MTAP deletion occurs in ~40% of mesothelioma and glioblastoma, ~20% of pancreatic cancer and bladder cancer, ~15% of NSCLC.

PRMT5 (MTAP-deleted cancers): what it is and how drugs act on it · animated generic schematic, not to scale
  • Target · the protein and the cell it sits on
  • Drug · antibody, small molecule, cell or radioligand
  • Effect · signal, damage or kill

In plain words · An enzyme that cancers lacking the MTAP gene (about 10-15% of all tumours) depend on more than normal cells do; new inhibitors designed to exploit that difference are in late trials.

  1. 1 · What it is

    An enzyme that cancers lacking the MTAP gene (about 10-15% of all tumours) depend on more than normal cells do; new inhibitors designed to exploit that difference are in late trials.

  2. 2 · What goes wrong in cancer

    Type II protein arginine methyltransferase forming symmetric dimethylarginine on histones (H4R3, H3R8) and splicing factors (SmD3); essential for spliceosome function; MTA is a competitive SAM-site inhibitor accumulating when MTAP is lost.

  3. 3 · How drugs use it

    No product in this corpus aims at PRMT5 (MTAP-deleted cancers) yet. Inhibitors are shaped to fit the enzyme's active site so the reaction the cancer relies on stops.

Biology

Type II protein arginine methyltransferase forming symmetric dimethylarginine on histones (H4R3, H3R8) and splicing factors (SmD3); essential for spliceosome function; MTA is a competitive SAM-site inhibitor accumulating when MTAP is lost.

Where it is found
  • Mesothelioma (~40% MTAP deletion)
  • Glioblastoma (~40%)
  • Pancreatic adenocarcinoma (~20%)
  • Urothelial carcinoma (~20%)
  • NSCLC (~15%)
  • Cholangiocarcinoma, melanoma, sarcoma (subsets)
Class
enzyme · PRMT5

How common it is, by cancer

CancerPrevalenceSource
Mesothelioma
40%
Glioma & glioblastoma
40%
Pancreatic ductal adenocarcinoma
20%
Non-small-cell lung cancer
15%

Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.

Key papers

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Latest papers

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Latest papers · live from Europe PMC
Open in Europe PMC

Query for this target: (TITLE:"PRMT5" OR ABSTRACT:"PRMT5" OR TITLE:"MTAP-deleted cancers" OR ABSTRACT:"MTAP-deleted cancers") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about PRMT5 (MTAP-deleted cancers), not a curated reading list.

Connected

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