OncoSignal
Live from Open Targets Platform, fetched 2026-11-11 16:09 UTC. Every row links to its source record.

CTNNB1 catenin beta 1

ENSG00000168036 · protein coding · Open Targets profile

Key downstream component of the canonical Wnt signaling pathway (PubMed:17524503, PubMed:18077326, PubMed:18086858, PubMed:18957423, PubMed:21262353, PubMed:22155184, PubMed:22647378, PubMed:22699938). In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N- terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome (PubMed:17524503, PubMed:18077326, PubMed:18086858, PubMed:18957423, PubMed:21262353, PubMed:22155184, PubMed:22647378, PubMed:22699938). In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes (PubMed:17524503, PubMed:18077326, PubMed:18086858, PubMed:18957423, PubMed:21262353, PubMed:22155184, PubMed:22647378, PubMed:22699938). Also acts as a coactivator for other transcription factors, such as NR5A2 (PubMed:22187462). Promotes epithelial to mesenchymal transition/mesenchymal to epithelial transition (EMT/MET) via driving transcription of CTNNB1/TCF-target genes (PubMed:29910125). Involved in the regulation of cell adhesion, as component of an E-cadherin:catenin adhesion complex (By similarity). Acts as a negative regulator of centrosome cohesion (PubMed:18086858). Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization (PubMed:21262353). Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2 (PubMed:18957423). Disrupts PML function and PML- NB formation by inhibiting RANBP2-mediated sumoylation of PML (PubMed:22155184). Promotes neurogenesis by maintaining sympathetic neuroblasts within the cell cycle (By similarity). Involved in chondrocyte differentiation via interaction with SOX9: SOX9-binding competes with the binding sites of TCF/LEF within CTNNB1, thereby inhibiting the Wnt signaling (By similarity). Acts as a positive regulator of odontoblast differentiation during mesenchymal tooth germ formation, via promoting the transcription of differentiation factors such as LEF1, BMP2 and BMP4 (By similarity). Activity is repressed in a MSX1-mediated manner at the bell stage of mesenchymal tooth germ formation which prevents premature differentiation of odontoblasts (By similarity). {ECO:0000250|UniProtKB:Q02248, ECO:0000269|PubMed:17524503, ECO:0000269|PubMed:18077326, ECO:0000269|PubMed:18086858, ECO:0000269|PubMed:18957423, ECO:0000269|PubMed:21262353, ECO:0000269|PubMed:22155184, ECO:0000269|PubMed:22187462, ECO:0000269|PubMed:22647378, ECO:0000269|PubMed:22699938, ECO:0000269|PubMed:29910125}.

In 11 of 15 cancers, the evidence for CTNNB1 comes mainly from mutations found in tumours

Each row is a cancer, strongest overall evidence first. The two dots show how strong the inherited (germline) and tumour-mutation (somatic) evidence is; the line between them is the gap.

Inherited (germline) variantsMutations in tumours (somatic)
00.250.50.751pilomatrixomapilomatrixomapilomatrixoma: somatic 0.79pilomatrixoma: germline 0.90hepatocellular carcinomahepatocellular carcinomahepatocellular carcinoma: somatic 0.86hepatocellular carcinoma: germline 0.85medulloblastomamedulloblastomamedulloblastoma: somatic 0.80medulloblastoma: germline 0.71ovarian cancerovarian cancerovarian cancer: somatic 0.55ovarian cancer: germline 0.80colorectal cancercolorectal cancercolorectal cancer: germline 0.76ovarian neoplasmovarian neoplasmovarian neoplasm: somatic 0.53ovarian neoplasm: germline 0.69hepatoblastomahepatoblastomahepatoblastoma: somatic 0.70prostate adenocarcinomaprostate adenocarcinomaprostate adenocarcinoma: somatic 0.73adrenal cortex carcinomaadrenal cortex carcinomaadrenal cortex carcinoma: somatic 0.70colon carcinomacolon carcinomacolon carcinoma: somatic 0.61colon carcinoma: germline 0.56endometrial cancerendometrial cancerendometrial cancer: somatic 0.81urinary bladder carcinomaurinary bladder carcinomaurinary bladder carcinoma: somatic 0.64non-small cell lung carcinomanon-small cell lung carcinomanon-small cell lung carcinoma: somatic 0.58colorectal adenocarcinomacolorectal adenocarcinomacolorectal adenocarcinoma: somatic 0.53urinary bladder cancerurinary bladder cancerurinary bladder cancer: somatic 0.68

Scores run from 0 (no evidence) to 1 (strongest). A missing dot at 0 means Open Targets holds no evidence of that kind. Source: Open Targets Platform, fetched live.

Tractability

Small molecule
Structure with Ligand, High-Quality Ligand, Druggable Family
Antibody
UniProt loc high conf, GO CC high conf, Human Protein Atlas loc
PROTAC
UniProt Ubiquitination, Database Ubiquitination, Half-life Data, Small Molecule Binder
Other modalities
Advanced Clinical

gnomAD loss of function constraint: o/e 0.07276800274848938 (upper bound 0.14361999928951263). Low values mean loss of function is poorly tolerated, a safety flag for inhibition.

Who runs trials of these drugs

No named investigators on registry trials of CTNNB1's approved or late-stage drugs in the last three years.

4 of 4 trials of drugs against CTNNB1 have sites only in Japan

Registry trials of PRI-724 updated in the last three years, counted by the country group of their listed sites. A trial with sites in several groups counts in each; 4 of 4 have all sites in one country.

Sites only in this groupSites here and elsewhere
JapanJapan: 4 trials with sites only hereJapan: 0 trials with sites here and elsewhere4

Site counts are not patients per country, and trials registered only outside ClinicalTrials.gov are not covered. Where sites are is a fact about the record, not a judgement of its quality. Europe is the EU and EEA, the UK and Switzerland. Source: ClinicalTrials.gov, fetched live.

2 trials of drugs against CTNNB1 were stopped early

Terminated, withdrawn and suspended interventional trials of PRI-724, newest update first, live from ClinicalTrials.gov. Each reason is quoted exactly as the registry gives it; we do not sort reasons into safety, efficacy or business. Dates are the last registry update. Showing the 2 most recent of 2.

  • terminated · 2017-08-17 · Prism Pharma Co., Ltd. · PRI-724
    “closing due to low enrollment, no safety issues”
  • withdrawn · 2017-04-17 · University of Southern California · CBP/beta-catenin Antagonist PRI-724
    “Study drug supply issues”
Paediatric incentives and obligations for CTNNB1's drugs

For PRI-724: what EMA and FDA publish about paediatric plans, orphan status and pediatric approvals, and how many registered studies take children. Each line is a yes, no or not published fact from the record linked under it; none of it is a forecast.

Rare pediatric disease voucher. FDA, content current as of 29 Apr 2026: “As of February 3, 2026, enactment of the Consolidated Appropriations Act, 2026, the rare pediatric disease PRV program will sunset after September 30, 2029. FDA may not award any PRVs under this program after September 30, 2029.” Voucher sale prices are not shown here; they appear only as company-reported news. FDA: Rare Pediatric Disease Designation and Priority Review Voucher Programs

All 1 drugs and clinical candidates as a table

Each drug, stage and indication links to its Open Targets record, where the trials and approvals behind it are listed. Salt forms (for example a mesylate) are listed as Open Targets records them, as separate entries.

DrugTypeHighest stageIndicationsSource records
PRI-724Unknownphase 2colorectal cancer, cirrhosis of liver, acute myeloid leukemia by FAB classification, acute myeloid leukemia, chronic myeloid leukemia, colorectal carcinoma, pancreatic adenocarcinomaOpen Targets · ChEMBL