Drug pipeline
Full profile accessExplore the programs pursuing this target and their development progress.
- Drug candidates
- Developers
- Development stage
Target intelligence / Profile preview
Traf2- and Nck-interacting protein kinase (TNIK) (TNIK)
- Target
- TNIK
- Molecular classification
- Enzyme, Serine/threonine protein kinase, Kinase (STE20/GCK family member)
01
Overview
Traf2- and Nck-interacting protein kinase (TNIK) is a serine/threonine kinase that serves as an essential activator of the Wnt signaling pathway by being recruited to promoters of Wnt target genes, interacting with β-catenin and TCF4, and phosphorylating TCF4 to drive TCF/LEF-dependent transcription; it also contributes to cytoskeletal regulation and broader signal transduction, has been implicated in cancers (notably Wnt-driven colorectal cancer), pulmonary fibrosis, and other conditions, and is under investigation as a therapeutic target with small-molecule inhibitors and mechanistic links to agents such as dovitinib
- Other names
- TRAF2 and NCK interacting kinaseTRAF-2 and NCK-interacting kinaseTNIK proteinSerine/threonine-protein kinase TNIKGene symbol: TNIK
02
Mechanism of action
Small-molecule TNIK inhibitors blocking TNIK kinase activity to suppress Wnt/β-catenin–dependent transcription and proliferation in Wnt-active cancer cells; Multikinase inhibitor dovitinib affecting pathways involving TNIK in anti-cancer activity in myeloma models (mechanistic involvement reported)
03
Biological functions
Signal transductionWnt/β-catenin pathway activation via TCF4 phosphorylation and β-catenin/TCF complex regulationGene transcription regulation of Wnt target genesCytoskeletal organization, including phosphorylation of gelsolin affecting F-actin dynamicsJNK pathway involvement (proposed)
04
Disease associations
Cancer, including Wnt-driven colorectal carcinogenesisPulmonary fibrosisNeurological disorders and inflammatory conditions (emerging research interest)Multiple myeloma growth signaling (IL-6–dependent proliferation implication)
05
Safety considerations
On-target risks from inhibiting Wnt signaling (potential effects on intestinal stem cell maintenance and tissue homeostasis)Limited clinical validation; few inhibitors and none advanced far preclinically as of reports, indicating development risk
06
Interacting drugs
Dovitinib (reported to involve TNIK in its anti-cancer mechanism in myeloma models)
1 more in the full profile.
07
Biomarkers
Wnt/β-catenin activation status or TCF/LEF target gene expression as pharmacodynamic markers for TNIK pathway inhibitionTNIK expression/activity levels in Wnt-driven tumors as exploratory biomarkers
Beyond the preview
Go deeper on Traf2- and Nck-interacting protein kinase (TNIK) (TNIK).
Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.
Clinical trials
Full profile accessFollow the clinical studies evaluating therapies directed at this target.
- Trial design
- Status
- Readouts
Competitive landscape
Full profile accessCompare approaches across drug candidates, modalities, and indications.
- Programs
- Modalities
- Indications
Literature & evidence
Full profile accessInvestigate the research and source evidence behind target biology and development.
- Publications
- Sources
- Analysis
Patents
Full profile accessExplore patent activity around therapies and technologies addressing this target.
- Patents
- Assignees
- Technologies
Research & analysis
Full profile accessConnect target biology, drug development, and emerging evidence in your research.
- Biology
- Development news
- Analysis
Bring the full picture into focus.
See how Gosset can support your research on Traf2- and Nck-interacting protein kinase (TNIK) (TNIK).