2-Hydroxy Imiquimod
2-Hydroxy Imiquimod (R-842), a hydroxylated metabolite of Imiquimod (HY-B0180), is an immunomodulating agent. 2-Hydroxy Imiquimod can induce IFN-α, TNF-α, IL-1, IL-6 and IL-8 in human blood cells. 2-Hydroxy Imiquimod exhibits antivirus and antitumor activities. 2-Hydroxy Imiquimod can be used for the researches of cancer, infection and immunology.
For research use only. We do not sell to patients.
- CAS No.: 112668-45-8
- Formula: C14H16N4O
- Molecular Weight:256.30
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
IL-1 |
IL-6 |
IL-8 |
Cellular Effect
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Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | EC50 |
>270 μM
Compound: 3
|
Agonist activity at human TLR8 transfected in HEK cells assessed as NFkappaB induction after 24 hrs by specific secreted alkaline phosphatase gene assay
Agonist activity at human TLR8 transfected in HEK cells assessed as NFkappaB induction after 24 hrs by specific secreted alkaline phosphatase gene assay
|
[PMID: 22837811] |
| HEK293 | EC50 |
95 μM
Compound: 3
|
Agonist activity at human TLR7 transfected in HEK cells assessed as NFkappaB induction after 24 hrs by specific secreted alkaline phosphatase gene assay
Agonist activity at human TLR7 transfected in HEK cells assessed as NFkappaB induction after 24 hrs by specific secreted alkaline phosphatase gene assay
|
[PMID: 22837811] |
Chemical Information
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CAS No. 112668-45-8
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Molecular Weight 256.30
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Formula C14H16N4O
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SMILES
OC(C)(CN1C=NC2=C1C3=C(C=CC=C3)N=C2N)C
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Synonyms
R-842
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. Weeks CE, et al. Induction of interferon and other cytokines by imiquimod and its hydroxylated metabolite R-842 in human blood cells in vitro. J Interferon Res. 1994 Apr;14(2):81-5. [Content Brief]
[2]. Imbertson LM, et al. Cytokine induction in hairless mouse and rat skin after topical application of the immune response modifiers imiquimod and S-28463. J Invest Dermatol. 1998 May;110(5):734-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)