DiMNF | AhR modulator (SAhRM)
NMR (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 10 mg | $50.00 | ||
| 50 mg | $190.00 |
DiMNF (14756-24-2) is a selective aryl hydrocarbon receptor (AHR) modulator (SAhRM). It exhibits antiinflammatory activity including suppression of cytokine-mediated acute phase genes through dissociation of non-dioxin-response element (DRE) AHR activity from DRE-dependent xenobiotic gene expression.1 DiMNF represses the cytokine-mediated induction of CD55 and therefore may have therapeutic potential in regulating the immune response to tumor formation.2 Represses estrogen-inducible transcription.3
References/Citations:
1) Murray et al. (2011), Suppression of cytokine-mediated complement factor gene expression through selective activation of the Ah receptor with 3’,4’-dimethoxy-α-naphthoflavone; Mol. Pharmacol., 79 508
2) Narayanan et al. (2012), Selective aryl hydrocarbon receptor modulator-mediated repression of CD55 expression induced by cytokine exposure; J. Pharmacol. Exp. Ther., 342 345
3) Labrecque et al. (2012), Distinct roles for aryl hydrocarbon receptor nuclear translocator and ah receptor in estrogen-mediated signaling in human cancer cell lines; PLoS One, 7(1) e29545
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
DiMNF (14756-24-2) is a selective aryl hydrocarbon receptor (AHR) modulator (SAhRM). It exhibits antiinflammatory activity including suppression of cytokine-mediated acute phase genes through dissociation of non-dioxin-response element (DRE) AHR activity from DRE-dependent xenobiotic gene expression.1 DiMNF represses the cytokine-mediated induction of CD55 and therefore may have therapeutic potential in regulating the immune response to tumor formation.2 Represses estrogen-inducible transcription.3
References/Citations:
1) Murray et al. (2011), Suppression of cytokine-mediated complement factor gene expression through selective activation of the Ah receptor with 3’,4’-dimethoxy-α-naphthoflavone; Mol. Pharmacol., 79 508
2) Narayanan et al. (2012), Selective aryl hydrocarbon receptor modulator-mediated repression of CD55 expression induced by cytokine exposure; J. Pharmacol. Exp. Ther., 342 345
3) Labrecque et al. (2012), Distinct roles for aryl hydrocarbon receptor nuclear translocator and ah receptor in estrogen-mediated signaling in human cancer cell lines; PLoS One, 7(1) e29545
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