# CDK9

Source: https://onco.cc/targets/cdk9/  
OnCo record `cdk9` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

CDK9 (Cyclin-dependent kinase 9) is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Hepatocellular carcinoma, Oesophageal cancer and Neuroblastoma.

## Summary

Protein kinase involved in the regulation of transcription. Member of the cyclin-dependent kinase pair (CDK9/cyclin-T) complex, also called positive transcription elongation factor b (P-TEFb), which facilitates the transition from abortive to productive elongation by phosphorylating the CTD (C-terminal domain) of the large subunit of RNA polymerase II (RNAP II) POLR2A, SUPT5H and RDBP. This complex is inactive when in the 7SK snRNP complex form.

CIViC holds 3 clinical evidence items and 0 assertions across 1 variant, naming Dinaciclib, Alvocidib and CAN508.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: cyclin dependent kinase 9; Cyclin-dependent kinase 9; PITALRE; C-2k; CDC2L4
- Tags: cancer-genes-wave
- Symbol: CDK9
- Class: kinase
- Biology: Protein kinase involved in the regulation of transcription. Member of the cyclin-dependent kinase pair (CDK9/cyclin-T) complex, also called positive transcription elongation factor b (P-TEFb), which facilitates the transition from abortive to productive elongation by phosphorylating the CTD (C-terminal domain) of the large subunit of RNA polymerase II (RNAP II) POLR2A, SUPT5H and RDBP. This complex is inactive when in the 7SK snRNP complex form. Phosphorylates EP300, MYOD1, RPB1/POLR2A and AR and the negative elongation factors DSIF and NELFE. Regulates cytokine inducible transcription networks by facilitating promoter recognition of target transcription factors (e.g. TNF-inducible RELA/p65 activation and IL-6-inducible STAT3 signalling). Location: Nucleus; Cytoplasm; Nucleus, PML body (UniProt). Locus 9q34.11 (HGNC).
- Where found: Hepatocellular carcinoma: CIViC evidence names this disease; Oesophageal cancer: CIViC evidence names this disease; Neuroblastoma: CIViC evidence names this disease

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC lists 3 therapies; CIViC holds 3 clinical evidence items on its variants; UniProt keyword "DNA repair". Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:1780: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:1780
- UniProt P50750: https://www.uniprot.org/uniprotkb/P50750/entry
- NCBI Gene 1025: https://www.ncbi.nlm.nih.gov/gene/1025
- Ensembl ENSG00000136807: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000136807

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/)
- cancers: [Hepatocellular carcinoma](https://onco.cc/cancers/hcc/), [Neuroblastoma (paediatric)](https://onco.cc/cancers/neuroblastoma/), [Oesophageal cancer](https://onco.cc/cancers/esophageal/)
- pathways: [MYC](https://onco.cc/pathways/myc/), [Transcriptional machinery & addiction](https://onco.cc/pathways/transcription-addiction/)
- trials: [Study of SLS009 (Formerly GFH009) a Potent Highly Selective CDK9 Inhibitor in Patients With Hematologic Malignancies and High-Risk Newly Diagnosed AML](https://onco.cc/trials/nct04588922/)

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