Arvanil | TRPV1 channel activator
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $40.00 | ||
| 25 mg | $135.00 |
Arvanil (128007-31-8) is a non-pungent capsaicin analog with antinociceptive and anti-inflammatory effects in vivo.1 It is an agonist at TRPV1 as well as CB1 (Ki = 0.25 – 0.52 μM), but not CB2.2,3 Caused high mitochondrial calcium flow in hepatocellular carcinoma cells, ultimately leading to ferroptosis.4 It induced FADD-dependent apoptosis in lymphoid Jurkat T-cells.5 Neuroprotective in rat excitotoxicity model.6
References/Citations:
- Janusz et al. (1993), 1. Analogs of capsaicin with antinociceptive and antiinflammatory activity; J. Med. Chem. 36 2595
- Lim et al. (2022), Highly Efficient Real-Time TRPV1 Screening Methodology for Effective Drug Candidates; ACS Omega 7 36441
- Di Marzo et al. (1998), Interactions between synthetic vanilloids and the endogenous cannabinoid system; FEBS Lett. 436 449
- Deng et al. (2024), Arvanil induces ferroptosis of hepatocellular carcinoma by binding to MICU1; Cancer Gene Ther. 31 148
- Sancho et al. (2003), The CB1/VR1 agonist arvanil induces apoptosis through an FADD/caspase-8-dependent pathway; Br. J. Pharmacol. 140 1035
- Veldhuis et al. (2003), Neuroprotection by the endogenous cannabinoid anandamide and arvanil against in vivo excitotoxicity in the rat: the role of vanilloid receptors and lipoxygenases; J. Neurosci. 23 4127
C28 H41NO3
>98% TLC
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
Arvanil (128007-31-8) is a non-pungent capsaicin analog with antinociceptive and anti-inflammatory effects in vivo.1 It is an agonist at TRPV1 as well as CB1 (Ki = 0.25 – 0.52 μM), but not CB2.2,3 Caused high mitochondrial calcium flow in hepatocellular carcinoma cells, ultimately leading to ferroptosis.4 It induced FADD-dependent apoptosis in lymphoid Jurkat T-cells.5 Neuroprotective in rat excitotoxicity model.6
References/Citations:
- Janusz et al. (1993), 1. Analogs of capsaicin with antinociceptive and antiinflammatory activity; J. Med. Chem. 36 2595
- Lim et al. (2022), Highly Efficient Real-Time TRPV1 Screening Methodology for Effective Drug Candidates; ACS Omega 7 36441
- Di Marzo et al. (1998), Interactions between synthetic vanilloids and the endogenous cannabinoid system; FEBS Lett. 436 449
- Deng et al. (2024), Arvanil induces ferroptosis of hepatocellular carcinoma by binding to MICU1; Cancer Gene Ther. 31 148
- Sancho et al. (2003), The CB1/VR1 agonist arvanil induces apoptosis through an FADD/caspase-8-dependent pathway; Br. J. Pharmacol. 140 1035
- Veldhuis et al. (2003), Neuroprotection by the endogenous cannabinoid anandamide and arvanil against in vivo excitotoxicity in the rat: the role of vanilloid receptors and lipoxygenases; J. Neurosci. 23 4127
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