pitavastatin

P1, N=32, Active, not recruiting, Genentech Inc. | Recruiting --> Active, not recruiting

P2, N=150, Recruiting, Lomonosov Moscow State University Medical Research and Educational Center

P1, N=40, Recruiting, Hoffmann-La Roche | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Jun 2026 --> Dec 2026

P=N/A, N=6927, Completed, JW Pharmaceutical

P4, N=88, Active, not recruiting, JW Pharmaceutical

P1, N=32, Recruiting, Genentech Inc.

Targeting this pathway with clinically approved statins (atorvastatin, pitavastatin, simvastatin) synergized with PT2385 to suppress CRC cell growth, reduce colony formation, and enhance cell death...These effects are fully reversed by the ferroptosis inhibitor liproxstatin-1...In vivo, co-administration of PT2385 and atorvastatin significantly reduced tumor growth and increased ferroptotic cell death in xenografts, confirming the mechanistic link. Collectively, these findings uncover a metabolic vulnerability of CRC to dual HIF-2α and cholesterol biosynthesis inhibition, supporting a clinically actionable strategy that leverages safe, FDA-approved statins to potentiate HIF-2α-targeted therapy.

P=N/A, N=22, Not yet recruiting, Shanghai Pulmonary Hospital; Shanghai Pulmonary Hospital

P3, N=300, Active, not recruiting, Kirby Institute | Recruiting --> Active, not recruiting

The RT-qPCR results of zebrafish verified that Pitavastatin inhibited the expression of HMGCR, while Cabazitaxel inhibited the expression of TUBB1. Our study suggested that Pitavastatin has therapeutic effects on OA, while Cabazitaxel increases the risk of OA.

Loss of p53 function is strongly associated with venetoclax resistance, and adding venetoclax to 5-azacitidine provides no overall survival benefit in TP53 -mutant AML. The pro-apoptotic actions of pitavastatin depend on depletion of geranylgeranyl pyrophosphate (GGPP) and can be recapitulated by inhibiting GGPP synthase or geranylgeranyltransferase-1 enzymes. These results provide a mechanistic rationale for adding pitavastatin to AML regimens to prevent or overcome venetoclax resistance.

In the ex vivo evaluations, pitavastatin (0.5004 μM), eltrombopag (0.2548 μM), flavoxate (0.1536 μM), and empagliflozin (0.2548 μM) affected the phosphorylation of downstream STAT1 and STAT3 signaling molecules, similarly to tofacitinib citrate (TOF) (1.2 nM ). These results encourage further in-depth preclinical experiments aimed at exploring the additional effects of the JAK2-STAT1/3 signaling pathway.