Imiquimod

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Imiquimod
Systematic (IUPAC) name
1-isobutyl-1H-imidazo[4,5-c]quinolin-4-amine
Identifiers
CAS number 99011-02-6
ATC code D06BB10
PubChem 57469
DrugBank APRD01030
Chemical data
Formula C14H16N4 
Mol. mass 240.304 g/mol
Pharmacokinetic data
Bioavailability  ?
Metabolism  ?
Half life 20 hours (topical dose), 2 hours (subcutaneous dose)
Excretion  ?
Therapeutic considerations
Licence data

EUUS

Pregnancy cat.

B1(AU) C(US)

Legal status

POM(UK) -only(US)

Routes Topical

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Imiquimod

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Overview

Imiquimod (INN, marketed by 3M under the trade name Aldara) is a prescription medication that acts as an immune response modifier.

Uses

Imiquimod is a patient-applied cream used to treat certain diseases of the skin, including skin cancer (basal cell carcinoma, Bowen's disease[1], superficial squamous cell carcinoma, some superfical malignant melanomas and actinic keratosis) as well as genital warts (Condylomata Acuminata). It has also been tested for treatment of Molluscum contagiosum. It causes interferon production which triggers the patient's immune response against these tumors.

It is also used pre-operatively to shrink basal cell cancer and melanoma in situ (especially Lentigo Maligna) before Mohs surgery.

Side effects include redness and irritation of the skin during treatment.

History

The original FDA approval was on February 27, 1997, FDA Application No. (NDA) 020723, by Graceway.

Since then, the label has been revised many times. Adverse side effects have been reported, in some cases serious and systemic. Some patients have been suffering from severe auto-immune or neuro-immune effects for years.[citation needed]

Mechanism of action

The exact mode in which imiquimod and its analogs activate the immune system is not yet known. Nevertheless, it is known that Imiquimod activates immune cells by ligating the toll-like receptor 7 (TLR7), commonly involved in pathogen recognition, on the cell surface.[1] Cells activated by imiquimod via TLR-7 secrete cytokines (primarily interferon-α (IFN-α), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)). [1] There is evidence that imiquimod, when applied to skin, can lead to the activation of Langerhans cells, which subsequently migrates to local lymph nodes to activate the adaptive immune system.[1] Other cell types activated by imiquimod include natural killer cells, macrophages and B-lymphocytes.[1]

References


External links

de:Imiquimod

nl:Imiquimodth:อีมิควิมอด

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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