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Imiquimod hydrochloride

Catalog No.
B1186
Toll-like receptor 7 agonist
Grouped product items
SizePriceStock Qty
100mg
$50.00
In stock
For scientific research use only and should not be used for diagnostic or medical purposes.

Tel: +1-832-696-8203

Email: [email protected]

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Background

Imiquimod hydrochloride is an immune response modifier that acts as a toll-like receptor 7 agonist and is commonly used topically to treat warts on the skin of the genital and anal areas.

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
M.Wt276.76
Cas No.99011-78-6
FormulaC14H17ClN4
Solubility≥3.59 mg/mL in EtOH with ultrasonic; ≥5.54 mg/mL in DMSO with gentle warming and ultrasonic; ≥7.34 mg/mL in H2O with ultrasonic
Chemical Name1-isobutyl-1H-imidazo[4,5-c]quinolin-4(5H)-imine hydrochloride
SDFDownload SDF
Canonical SMILESCC(CN1C=NC2=C1C3=CC=CC=C3NC2=N)C.Cl
Shipping ConditionSmall Molecules with Blue Ice, Modified Nucleotides with Dry Ice.
General tips We do not recommend long-term storage for the solution, please use it up soon.

Protocol

Cell experiment:[1]

Cell lines

Thioglycollate-elicited peritoneal cells from wild-type (C57BL/6) and MyD88-deficient mice

Reaction Conditions

101 ~ 104 nM imiquimod for 24 h incubation

Applications

Imiquimod increased TNF-α and IL-12p40 production in IFN-γ-treated murine peritoneal macrophages in a concentration- and MyD88-dependent manner.

Animal experiment:[2]

Animal models

Female Hartley guinea pigs, 400 ~ 500 g

Dosage form

5 mg/kg

Administered intravaginally every 12 h for five days beginning 12 h after genital HSV-2 inoculation

Applications

Imiquimod (5 mg/kg, intravaginally, twice daily) reduced vaginal viral titer and lesion formation in a guinea pig model of genital HSV-2 infection. Imiquimod exhibited potent anti-HSV activity in vivo due to cytokine induction and enhancement of cell-mediated responses.

Note

The technical data provided above is for reference only.

References:

1. Hemmi H, Kaisho T, Takeuchi O, et al. Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway. Nature Immunology, 2002, 3(2): 196-200.

2. Harrison CJ, Jenski L, Voychehovski T, et al. Modification of immunological responses and clinical disease during topical R-837 treatment of genital HSV-2 infection. Antiviral Research, 1988, 10(4-5): 209-223.

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