Dyclonine

Dyclonine selectively inhibits purified TRPV3 channels with an IC₅₀ of 3.2 μM; it inhibits purified ALDH2 with an IC₅₀ of 35 μM; it also inhibits purified ALDH3A1 with an IC₅₀ of 76 μM; and it potently and selectively inhibits purified AchE in a non-competitive manner with an IC₅₀ of 0.18 μM^[1].
Dyclonine inhibits the proliferation of cultured cardiomyocytes at concentrations of 1-10 μM by suppressing ALDH2; it also inhibits the proliferation of HSC4 oral squamous cell carcinoma cells cultured in vitro, and restores the sensitivity of drug-resistant HSC4 cells to Sulfasalazine (HY-14655) via ALDH inhibition^[1].
Dyclonine (0.3-10 μM; 48 h) dose-dependently increases the FXN protein level in lymphoblasts derived from Friedreich's ataxia (FA)^[2].
Dyclonine (3-30 μM; 24 h) dose-dependently increases the level of FXN transcripts in lymphoblasts derived from Friedreich's ataxia (FA) patients, reaching a maximum induction of approximately 3.2-fold after treatment with 30 μM for 24 h, and exhibits a stronger inductive effect in cells with longer GAA repeat sequences^[2].
Dyclonine (5 μM; 24 h) enhances the binding of Nrf2 to the conserved ARE site in the FXN locus in lymphoblasts from FA patients^[2].
Dyclonine (1-10 μM) dose-dependently inhibits the activity of histone methyltransferase G9a in nuclear extracts of healthy lymphoblasts; it also rescues the aconitase activity defect in lymphoblasts derived from Fanconi anemia (FA)^[2].
Dyclonine (3-30 μM; with 1 mM 2-APB (HY-W009724)) modulates the inhibitory potency against mouse TRPV3 channels overexpressed in HEK 293T cells, and this regulatory effect relies on amino acid residues located in the channel pore region. Relative to wild-type TRPV3 with an IC₅₀ value of 3.2 μM, L630W, N643A, I644W and L655A mutations reduce its inhibitory capacity, whereas L642A and I659A mutations strengthen its channel-blocking activity^[3].
Dyclonine (15 μM) enhances the cytotoxic effect of 40 nM Bortezomib (HY-10227), reduces the survival rate of drug-resistant RPMI8226.BR multiple myeloma cells by approximately 80%, and induces cell apoptosis; it also enhances the cytotoxic activity of MG132 (HY-13259), inhibits the proliferation of BT549 and MDA-MB-231 breast cancer cells, and induces their apoptosis^[1].
Dyclonine inhibits the growth of Saccharomyces cerevisiae in vitro, and exerts a synergistic effect with Calyculin A (HY-18983) to enhance this effect by targeting sterol biosynthetic enzymes including Erg2p and ERG24^[1].
Dyclonine increases mitochondrial ATP production in cultured primary neurons and enhances their spontaneous excitatory postsynaptic current activity; it also inhibits the formation of Aβ42 oligomers in vitro^[1].
Dyclonine potently protects fibroblasts derived from Fanconi anemia (FA) from diamide-induced oxidative stress, with an EC₅₀ of approximately 0.2 μM^[2].
Dyclonine (1.25-10 μM; 24 h) dose-dependently activates the Nrf2/ARE pathway in stable HeLa-ARE-luciferase cells, and luciferase activity is induced to approximately 2.5-fold after treatment with 10 μM for 24 h^[2].

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