In vivo, endothelial GPRC5B deficiency significantly accelerated tumor growth and neovascularization, phenotypes that were effectively reversed by the p38 inhibitor SB202190. Clinical specimens corroborated reduced GPRC5B expression and increased microvessel density in MetS-associated PCa. Collectively, our findings establish endothelial GPRC5B downregulation as a key molecular driver promoting pathological angiogenesis via the MKK3/6-DUSP1-p38 axis, suggesting that targeting this signaling cascade offers a promising therapeutic strategy for managing MetS-associated PCa aggression.

The p38 MAPK inhibitor SB202190 reversed ORI-induced effects on cell death, cell migration and invasion, and apoptosis, highlighting the critical role of the p38 MAPK/p53 pathway. ORI effectively suppressed subcutaneous tumour growth in nude mice without notable toxicity while upregulating apoptosis-related proteins Bax and cleaved caspase-3 and downregulating Bcl-2 through activation of the p38 MAPK/p53 pathway.

Pharmacodynamic findings confirm that POLB 001 inhibits LPS-induced local and systemic inflammation in vivo through inhibition of p38 MAPK. https://onderzoekmetmensen.nl/en/trial/51741, identifier NL81214.056.22.

These results suggest that BMP-7 might inhibit PON-induced cardiotoxicity. Furthermore, our findings pave the way for future translational studies with BMP-7, which can demonstrate the therapeutic potential of BMP-7 in a clinical setting.

P1, N=6, Recruiting, GEn1E Lifesciences | Not yet recruiting --> Recruiting

Therefore, Viscosalactone B and Withasomniferol C are promising natural candidates for further validation as potential MAPK14 inhibitors. In comparison with synthetic drugs like ralimetinib, these plant-derived compounds may offer complementary therapeutic potential with fewer adverse or off-target effects and favorable pharmacokinetic and pharmacophoric profiles.

Pretreatment with the inhibitor SB202190 decreased the expression of proteins related to Ras/Raf/p38 MAPK and significantly suppressed the proliferation, migration, and invasion of A549 cells...NFATc1 is highly expressed in LUAD tissues, and its expression level is closely related to clinical characteristics. NFATc1 may promote the proliferation, migration, and LUAD cell invasion via the Ras/Raf/p38 MAPK pathway, providing a new therapeutic target for LUAD.

The mice in the anti-p38MAPK group and the anti-p38MAPK + LV-OPN-0423 group were then given SB202190 (this is an inhibitor of p38MAPK) for 4 weeks, and the mice in each group were injected with corresponding lentivirus diluent once a week for 8 weeks...The OPN level promoted the expression of p38MAPK and p-p38MAPK. These results suggested that OPN could regulate Em's growth and metastasis through the p38MAPK signalling pathway in host hepatocytes, providing evidence that OPN and p38MAPK may be novel molecular targets for treating alveolar echinococcosis.

P1/2, N=70, Active, not recruiting, Dan Zandberg | Trial completion date: Oct 2025 --> Dec 2025

P2, N=52, Recruiting, GEn1E Lifesciences | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Oct 2025 --> Oct 2026

P2, N=25, Active, not recruiting, EIP Pharma Inc | Recruiting --> Active, not recruiting

P1, N=6, Not yet recruiting, GEn1E Lifesciences