Diprovocim-1 is a highly potent, small-molecule TLR1/TLR2 dual agonist with an EC₅₀ of 110 pM for human TLR1/TLR2. Diprovocim-1 can be used in research on immunological adjuvants and anticancer vaccines.

Methods: MODE-K cells were treated with Diprovocim-1 (0.5 μM) for 12 hours, followed by irradiation with ⁶⁰Co γ-rays (6 Gy). Western blot analysis was performed to detect the expression of TLR2, MyD88, p-p38, p-JNK, and p-ERK.
Results: Diprovocim-1 upregulated TLR2 and MyD88 expression and activated the MAPK pathway. [1]
Methods: OVA-Cy5 (5 μg) or Diprovocim-1 (1 μM) was added to JAWSII (DC line), RAW264.7 (macrophage line), and mouse bone marrow-derived DCs, and the cells were incubated for 24 h. Cy5 MFI was quantified by flow cytometry and immunofluorescence.
Results: Diprovocim-1 significantly enhanced the uptake of OVA-Cy5 by JAWSII and RAW264.7 cells.[2]

Methods: Male C57BL/6 mice were subjected to whole-body irradiation with ⁶⁰Co γ-rays (7.5 Gy or 12 Gy). Diprovocim-1 (10 mg/kg) or saline was administered intraperitoneally 18 hours and 2 hours prior to irradiation. Body weight was measured daily for 5 days post-irradiation, and Kaplan-Meier survival curves were analyzed.
Results: Diprovocim-1 significantly prolonged survival time in mice following 7.5 Gy and 12 Gy irradiation and attenuated weight loss in mice following 12 Gy irradiation. [1]
Methods: C57BL/6 mice were immunized via the intranasal or intramuscular route, with a total of 3 doses administered at 2-week intervals. The mice were divided into OVA (30 μg) alone and OVA + Diprovocim-1 (30 μg) groups. Samples were collected 24 hours after a single administration.
Results: Diprovocim-1 significantly enhanced the ability of antigen-specific CD4⁺ and CD8⁺ T cells to produce IFN-γ and TNF-α.[2]

H2O: < 1?mg/mL?(insoluble)

DMSO: 26.66 mg/mL (29.33 mM), Sonication is recommended.