1. Membrane Transporter/Ion Channel Anti-infection Neuronal Signaling
  2. Fungal Calcium Channel
  3. Suloctidil hydrochloride

Suloctidil hydrochloride is an orally active calcium channel blocker and antifungal agent. Suloctidil hydrochloride antagonizes vasoconstriction induced by norepinephrine, angiotensin and serotonin. Suloctidil hydrochloride inhibits platelet function and exhibits neuroprotective effects. Suloctidil hydrochloride exerts inhibitory effects on Candida albicans biofilm and virulence. Suloctidil hydrochloride can be used in research on vasospasm relief, antithrombosis and superficial candidiasis.

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Suloctidil hydrochloride

Suloctidil hydrochloride Chemical Structure

CAS No. : 54767-71-4

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Description

Suloctidil hydrochloride is an orally active calcium channel blocker and antifungal agent. Suloctidil hydrochloride antagonizes vasoconstriction induced by norepinephrine, angiotensin and serotonin. Suloctidil hydrochloride inhibits platelet function and exhibits neuroprotective effects. Suloctidil hydrochloride exerts inhibitory effects on Candida albicans biofilm and virulence. Suloctidil hydrochloride can be used in research on vasospasm relief, antithrombosis and superficial candidiasis[1][2][3].

In Vitro

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Real Time qPCR[1]

Cell Line: Candida albicans strain YEM30
Concentration: 4 μg/mL
Incubation Time: 18 h
Result: Reduced the expression of hypha-specific genes HWP1 by 2.8-fold, ALS3 by 2.3-fold, and ECE1 by 4.9-fold compared to untreated controls.
In Vivo

Suloctidil (256 μg/mL; intravaginal; daily; until day 21 post-infection) hydrochloride significantly reduces C. albicans fungal burden and attenuates vaginal tissue inflammation in a murine model of vulvovaginal candidiasis[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Kunming mice (female, 7-8 weeks old, 28-32 g, pseudoestrus via subcutaneous estradiol benzoate, intravaginally infected with Candida albicans)[1]
Dosage: 256 μg/mL
Administration: intravaginal; daily; until day 21 post-infection
Result: Significantly reduced C.
albicans fungal burden compared to vehicle controls, with statistically significant differences starting at day 5 post-infection, and sustained through day 15 post-infection.
Showed no detectable inflammatory cell infiltration in vaginal tissues at day 5 post-infection, while vehicle-treated mice had large amounts of neutrophil and mononuclear cell infiltration.
Exhibited only mild histologic changes at day 9 post-infection, compared to significant lymphocyte and mononuclear cell infiltration in vehicle-treated mice.
Had less lymphocyte and cellular infiltration in the mucosa propria than vehicle-treated mice at day 15 post-infection.
Molecular Weight

374.02

Formula

C20H36ClNOS

CAS No.
SMILES

[H]Cl.O[C@H]([C@H](NCCCCCCCC)C)C1=CC=C(SC(C)C)C=C1

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Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Suloctidil hydrochloride
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