Arvanil

Arvanil (N-Vanillylarachidonamide) is a mixed agonist of CB1 and TRPV1 receptors. Arvanil downregulates CD25, HLA-DR, CD134/OX40, blocks G1/S phase transition, and induces phosphorylation of Akt. Arvanil does not induce apoptosis in cells. Arvanil inhibits lymphocyte activation and ameliorates autoimmune encephalomyelitis. Arvanil can be used in research related to Huntington's disease, vomiting, and multiple sclerosis^[1][2][3]. IC50 & Target:VR1, CB1^[1] In Vitro:Arvanil (10 μM; 48 h) potently inhibits the proliferation of OKT3-stimulated peripheral blood mononuclear cells (PBMCs), with an inhibition rate of 75.3% at 10 μM, and this effect is superior to that of anandamide and capsaicin at the same concentration^[3].
Arvanil (0.3-30 μM; 48 h) inhibits the proliferation of CD3CD28-stimulated human peripheral blood mononuclear cells (hPBMCs) in a dose-dependent manner, with an inhibition rate of 64.0% at 10 μM. It also reduces IFN-γ production, but does not affect IL-5 levels at this concentration^[3].
Arvanil (3-10 μM; 48 h) inhibits the proliferation of mouse CTLL-2 cells stimulated by IL-2, and significant inhibitory effect is observed at the concentration of 10 μM^[3].
Arvanil (10 μM) inhibits the upregulation of CD25, HLA-DR and CD134/OX40 activation markers on CD4⁺ T cells in OKT3-stimulated human peripheral blood mononuclear cells (hPBMCs)^[3].
Arvanil (10 μM; 48 h) does not induce apoptosis in CD4⁺ T cells derived from OKT3-stimulated human peripheral blood mononuclear cells (hPBMCs)^[3].
Arvanil (10 μM; 48 h) blocks G1/S phase transition in OKT3-stimulated human peripheral blood mononuclear cells (hPBMCs)^[3]. In Vivo:Arvanil (2 mg/kg; i.p.; single acute dose) alleviates hyperkinetic symptoms (increased ambulation, reduced inactivity) in a rat model of Huntington’s disease, an effect associated with increased glutamate content in the globus pallidus, while also reducing locomotor activity in normal rats^[1].
Arvanil (2 mg/kg; i.p.; single acute dose) reduces locomotor and exploratory activity in normal rats, an effect associated with increased GABA content in the globus pallidus^[1].
Arvanil (1-2 mg/kg; i.p.; single dose 15 min pre-M6G) dose-dependently inhibits morphine 6 glucuronide-induced emesis and vomiting in ferrets via activation of both CB₁ and TRPV₁ receptors, with the 2 mg/kg dose producing a significant reduction in emetic and vomiting episodes that is reversed by selective antagonists of these receptors^[2].
Arvanil (0.5 mg/kg; given on 2 separate days: day -3 and day +3 relative to EAE induction) treatment significantly ameliorates experimental autoimmune encephalomyelitis in female SJL/J mice, reducing the cumulative disease index by 48.2%, peak clinical score by 56.7%, maximal body weight loss by 66.8%, and central nervous system inflammatory foci by 51.3%^[3].