灵菌红素

Prodigiosin (25-500 nM; 24 hours) treatment reduces the viability of breast cancer cells, with IC ₅₀ values at 48 h of 62.52 nM in MDA-MB-231 cells and 261.2 nM in MDA-MB-468 cells.
Prodigiosin (25-500 nM; 24 hours) treatment significantly reduces the levels of phosphorylated LRP6 and DVL2, active β-catenin, and total β-catenin. Prodigiosin noticeably inhibits the phosphorylation of GSK3β at Ser9 in HEK293T cells, which is indicative of an increase in GSK3β activity.
Prodigiosin can inhibit proliferation and induce apoptosis in breast cancer cells.
Prodigiosin (25-500 nM; 24 hours) treatment dose-dependently blocks Wnt signaling activated by Wnt1, Wnt3, Wnt1/LRP6, Wnt3/LRP6, and Dishevelled 2 (DVL2) in transfected HEK293T cells. Prodigiosin treatment inhibits Wnt3A-CM-induced transcription in a dose-dependent manner. Prodigiosin inhibits transcription of the SuperTopFlash reporter activated by either Wnt transfection or Wnt3A treatment.
When applied to cultures of chytrid fungi Batrachochytrium dendrobatidis and B. salamandrivorans , Prodigiosin causes significant growth inhibition, with MIC values of 10 μM and 50 μM, respectively.

Prodigiosin (5 mg/kg; intraperitoneal injection; twice weekly; for 3 weeks) treatment significantly inhibits tumor growth. Prodigiosin treatment decreases tumor cell density and expression of the proliferation marker Ki-67.