Suloctidil hydrochloride

Suloctidil (4 μg/mL; 48 h) hydrochloride inhibits 80% of planktonic growth of Candida albicans strains YEM30 and LC3 with an MIC₈₀ of 4 μg/mL after 48 h of incubation^[1].
Suloctidil (4-32 μg/mL; 3-24 h) hydrochloride inhibits 80% of biofilm formation in Candida albicans strains YEM30 and LC3 with a BIC₈₀ of 16 μg/mL after 24 h, and exerts concentration-dependent, time-dependent biofilm formation inhibition, with complete inhibition at 16 and 32 μg/mL within 3 h^[1].
Suloctidil (32-256 μg/mL; 0.5-24 h) hydrochloride eradicates 80% of preformed biofilms in Candida albicans strains YEM30 and LC3 with a BEC₈₀ of 64 μg/mL after 24 h, and exerts rapid, concentration-dependent eradication activity, achieving a fungicidal endpoint within 0.5 h at 64, 128, and 256 μg/mL^[1].
Suloctidil (64 μg/mL; 1-24 h) hydrochloride induces time-dependent morphological damage to preformed Candida albicans YEM30 biofilms, with slight shrinkage at 1 h and severe shriveling and detachment at 24 h^[1].
Suloctidil (16 μg/mL; 12 h) hydrochloride completely inhibits yeast-to-hyphal switching in Candida albicans YEM30 when added at the start of culture, partially inhibits switching when added after 2 h, and does not inhibit switching when added after 4 h, following 12 h total incubation^[1].
Suloctidil (4 μg/mL; 18 h) hydrochloride downregulates the expression of hypha-specific genes HWP1, ALS3, and ECE1 in Candida albicans YEM30 by 2.8-, 2.3-, and 4.9-fold, respectively, after 18 h of incubation^[1].
Suloctidil (0.01-1 μM) hydrochloride non-competitively inhibits norepinephrine-, angiotensin-, and serotonin-induced contractions and competitively inhibits calcium-induced contractions in isolated arteries^[3].

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