Mirodenafil

Research use only, not for human use.

Mirodenafil is a PDE-5 inhibitor developed for the treatment of erectile dysfunction.The pharmacoki-netics of mirodenafil were not significantly altered by this concurrent administration. Mirodenafil (50 or 100 mg), obviously improved erectile function and was well tolerated in a representative population of Korean men with broad-spectrum ED of various etiologies and severities.

Mirodenafil is a PDE-5 inhibitor developed for the treatment of erectile dysfunction.The pharmacoki-netics of mirodenafil were not significantly altered by this concurrent administration. Mirodenafil (50 or 100 mg), obviously improved erectile function and was well tolerated in a representative population of Korean men with broad-spectrum ED of various etiologies and severities. Mirodenafil administered with alcohol had a tolerability profile comparable to that of mirodenafil alone. The concurrent administration of mirodenafil with alcohol was not associated with clinically significant hemodynamic changes in these healthy male volunteers in Korea. The coadministration of ketoconazole and rifampicin resulted in significant changes in systemic exposure to mirodenafil, in these healthy Korean male volunteers.

Mirodenafil (0-40 μM, 24 h) exerts neuroprotective functions via activating the cGMP/PKG/CREB signaling pathway.Mirodenafil (0-40 μM, 24 h) enhances neuronal survival by protecting the mitochondrial membrane potential and inhibiting apoptosis.Mirodenafil (0-40 μM) inhibits GSK-3β signaling, resulting in reduced tau phosphorylation, decreased Aβ production by inhibiting amyloidogenesis and activating the autophagosomal pathway.Mirodenafil inhibits the transcriptional activity of the glucocorticoid receptor (GR), and inhibits homodimerization of GR in HT-22 cells.Mirodenafil (0-100 μM, 24 h) inhibits TGF-β-induced phosphorylation of Smad2/3 and mRNA expression of the fibrosis marker in fibroblasts. Western Blot Analysis Cell Line:SH-SY5Y human neuroblastoma cells Concentration:0, 10, 20, 40 μM Incubation Time:24 h Result:Significantly increased cGMP levels by about 200% in a dose-dependent manner. Reversed the Aβ-induced decrease in phosphorylated CREB in a dose-dependent manner. Aβ42 alone increased the levels of cleaved caspase-3 and cleaved PARP, whereas the combined treatment with mirodenafil markedly reduced the expression levels of both apoptotic markers.RT-PCR Cell Line:NIH3T3 mouse embryonic fibroblasts Concentration:0, 10, 100 μM Incubation Time:24 h Result:The mRNA expression of COL1A1, α-SMA, and CTGF were induced by treatment with TGF-β1, and Mirodenafil significantly reduced the expression of these profibrotic genes.

Mirodenafil (4 mg/kg, IP, daily for 4 weeks) enhances the cognitive-behavioral performance in transgenic AD mice.Mirodenafil (0-10 mg/kg, Orally, daily for 3 weeks) ameliorates dermal fibrosis in a BLM-induced SSc mouse model by inhibiting the TGF-β signaling pathway, thereby suppressing the expression of collagen and profibrotic genes. Animal Model:APP-C105 transgenic mice (13-month-old, male, n=6)Dosage:4 mg/kgAdministration:IP, daily for 4 weeks Result:Improved cognitive function in the APP-C105 AD mice.Animal Model:Male BALB/c mice (8 weeks old, four groups, n=10/group)Dosage:0, 5 or 10?mg/kg Administration:Orally, daily for 3 weeks Result:Ameliorated dermal fibrosis and downregulated the protein levels of fibrosis markers including COL1A1 and α-SMA in the BLM-induced SSc mouse model. Significantly decreased dermal thickness and collagen content.

SK3530

Angiogenesis

PDE

PDE5

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862189-95-5

531.67

C26H37N5O5S

>98% (HPLC)

In Vitro:?DMSO : 125 mg/mL (235.11 mM)

CCCOc1ccc(cc1-c1nc2c(CCC)cn(CC)c2c(=O)[nH]1)S(=O)(=O)N1CCN(CCO)CC1

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(-20℃)

With Ice Pack

≥ 2 years