Diprovocim

Diprovocim is a potent TLR1/TLR2 agonist. Diprovocim elicits full agonist activity in human THP-1 cells (EC₅₀=110 pM). Diprovocim stimulates the release of TNF-α from mouse macrophages (EC₅₀=1.3 nM). Diprovocim activates downstream MAPK and NF-κB signaling pathway. Diprovocim displays strong adjuvant activity in mice, particularly abetting cellular immune responses^[1][2]. In Vitro:Diprovocim (5 nM in THP-1 and 500 nM in mouse peritoneal macrophage; 15-120 mins) induces phosphorylation of IKKα, IKKβ, p38, JNK, and ERK, as well as degradation of IκBα in THP-1 cells and mouse peritoneal macrophages^[2].
Diprovocim (0.01-10000 nM; 4 hours) induces dose-dependent TNF production by THP-1 cells (EC₅₀=110 pM) and human peripheral blood mononuclear cells (PBMC) (EC₅₀=875 pM) and by mouse peritoneal macrophages (EC₅₀=1.3 nM) and bone marrow-derived dendritic cells (BMDC) (EC₅₀=6.7 nM). In addition to TNF, Diprovocim induced IL-6 production by mouse BMDC^[2].
In Vivo:Diprovocim (10 mg/kg) uses as an adjuvant and mixed with ovalbumin (OVA; 100 μg) by i.m. induces similar levels of serum OVA-specific IgG after 14 days^[2].
Diprovocim (10 mg/kg; i.m.) mixed with ovalbumin (OVA; 100 μg) before inoculation with B16-OVA cells immunizes significantly slows tumor growth rate but failed to prolong survival relative to OVA alone after 7 days^[2].