| Identification | Back Directory | [Name]
DRACORHODIN PEROCHLORATE | [CAS]
125536-25-6 | [Synonyms]
Dracohodin perochlorate
Dracorhodin perchlorate
DRACORHODIN PEROCHLORATE
7-Hydroxy-5-methoxy-6-methyl-2-phenyl-1-benzopyrylium perchlorate | [Molecular Formula]
C17H15ClO7 | [MDL Number]
MFCD07781413 | [MOL File]
125536-25-6.mol | [Molecular Weight]
366.75 |
| Chemical Properties | Back Directory | [storage temp. ]
Amber Vial, -20°C Freezer, Under inert atmosphere | [solubility ]
DMSO (Slightly), Methanol (Slightly) | [form ]
Solid | [color ]
Very Dark Orange | [Stability:]
Moisture Sensitive |
| Hazard Information | Back Directory | [Uses]
Dracorhodin Perchlorate is an apoptotic agent, inducing apoptosis in fibroblasts from human skin hypertrophic scars. Antioxidant. | [in vivo]
Dracorhodin perchlorate (2.5-10 μg/mL；applied as an ointment；twice daily；0-14 days) promotes wound healing in rats, as evidenced by increased wound healing rate, enhanced fibroblast proliferation in wound tissue, and up -regulation of phosphorylated-ERK in wound tissue[3].
Dracorhodin perchlorate (200 μg/mL; topical application) promotes skin wound healing, collagen deposition, and microvascular formation in diabetic rats by regulating the TLR4 pathway and related inflammatory factors[6].
Dracorhodin perchlorate (5-20 mg/kg; i.p.; every other day; 30 d) lowers blood glucose, raises insulin levels, enhances Pdx1 expression, increases islet size and number, and shows protective effects on islets and β-cells in diabetic mice[7].
| Animal Model: | Male Sprague-Dawley rats (170-220 g, clean grade, 7-week-old approximately)+diabetes mellitus model induced by Streptozotocin (HY-13753) injection and high-fat diet[6] | | Dosage: | 200 μg/mL (dissolved in DMSO and made into ointment with Vaseline) | | Administration: | Topical application | | Result: | Accelerated the wound healing in diabetic rats.
Increased the wound healing rate.
Promoted collagen deposition and inhibited scar formation.
Increased the number of microvessels.
Reduced the activation of the TLR4 pathway, decreased the mRNA and protein expressions of inflammatory factors, increased eNOS protein expression and NO content in the later stage of wound healing.
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| [IC 50]
TLR4; Caspase 3 |
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