Prostate cancer often involves dysregulated signaling pathways, and one significant culprit is PIM-1 kinase. This constitutively active Serine/Threonine kinase contributes to tumor growth, therapy resistance, and poor prognosis. Finding a safe and effective PIM-1 inhibitor could offer new therapeutic options, especially for advanced or resistant prostate cancer.

Developing new drugs is costly and time-consuming. Repurposing approved medications—such as rifaximin—can accelerate the path to clinical use by leveraging known safety profiles. A recent study screened 3,800 FDA-approved drugs for PIM-1 inhibition, uncovering rifaximin as a promising lead compound.

Key Findings

• Molecular Docking and simulation showed that rifaximin binds and stably inhibits PIM-1 with an IC50 ~26 μM. IC50 is the concentration of a substance required to inhibit a specific biological or biochemical function by 50%.
• Stanozolol, telmisartan, and alfaxalone also bound PIM-1 in silico, but did not remain strongly bound in vitro.

Implications for Prostate Cancer

• Interrupting PIM-1 could slow or halt disease progression, especially in hormone-resistant cases.
• Rifaximin’s established safety could ease its transition into clinical trials, potentially broadening prostate cancer treatment strategies.
• It may be especially beneficial when combined with existing therapies to target multiple tumor survival pathways simultaneously.

In sum, repurposing rifaximin as a PIM-1 inhibitor holds exciting promise for prostate cancer by potentially improving outcomes and overcoming resistance to conventional treatments.

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