2-Guidinobenzimidazole rapidly inhibits proton transport in wild-type human Hv1 channels expressed in Xenopus oocytes by opening-channel blockade, exhibiting rapid binding and dissociation kinetics and not interacting with closed channels [2]. 2-Guidinobenzimidazole interacts with mutant human Hv1 channels (D112E, F150A) expressed in Xenopus oocytes via binding sites containing D112 and F150 residues, mutations at these sites altering the kinetics of rapid opening-channel blockade [2].

2-Guidinobenzimidazole (20 mg/kg; intraperitoneal injection; every other day) can activate tumor-associated inflammasomes, increase the number of tumor-infiltrating cytotoxic T cells, and significantly inhibit the growth of LLC tumors in C57BL/6J mice[1]. 2-Guidinobenzimidazole (20 mg/kg; intraperitoneal injection; every other day) can overcome anti-PD-1 resistance and exert a synergistic anti-tumor effect in C57BL/6J mice bearing LLC tumors[1]. 2-Guidinobenzimidazole (20 mg/kg; intraperitoneal injection; every other day) can significantly inhibit the growth of B16F10 melanoma in C57BL/6J mice[1]. 2-Guidinobenzimidazole (20 mg/kg; intraperitoneal injection; every other day) can activate inflammasomes, inhibit tumor growth, and enhance the anti-tumor immunity of LLC tumor mice in an NLRP3-dependent manner[1].

Animal/Disease Models:C57BL/6J (8-12 weeks old; subcutaneous injection of 1.5 × 10⁶ LLC cells) [1]
Doses: 20 mg/kg
Route of Administration: Intraperitoneal injection; every other day
Experimental Results: IL-1β levels in tumor tissue increased to approximately 2500 pg/mL/100 mg (n=7,8), and IL-18 levels increased to approximately 1500 pg/mL/100 mg (n=6). The proportion of caspase-1+ macrophages in tumors increased to 33.9% (n=6), the proportion of caspase-1+ dendritic cells increased to 32.8% (n=5), and the proportion of caspase-1+ neutrophils increased to 20.7% (n=5). After 30 days of treatment, the LLC tumor volume shrank to approximately 300 mm³ (n=6), and the tumor weight decreased to approximately 0.5 g (n=6). The tumor-infiltrating CD4+ T cell count increased to approximately 15 × 10⁵ (n=7), and the CD8+ T cell count increased to approximately 8 × 10⁵ (n=7). The percentage of IFN-γ+ CD8+ T cells increased to 17.5% (n=7). The migrating dendritic cell (DC) count increased to approximately 6 × 10³ (n=5), and the mean fluorescence intensity (MFI) of CD40 in DCs in the tumor-draining lymph nodes increased to approximately 1400, and the CD86 MFI increased to approximately 1600 (n=5). When administered alone, the LLC tumor volume shrank to approximately 400 mm³ after 30 days of treatment. When used in combination with an anti-PD-1 antibody, the tumor volume further shrank to approximately 200 mm³ after 30 days of treatment (n=5,6), overcoming anti-PD-1 resistance.

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Animal/Disease Models:C57BL/6J (8-12 weeks old; subcutaneous injection of 1.5 × 10⁶ B16F10 cells) [1]
Doses: 20 mg/kg
Route of Administration: Intraperitoneal injection; every other day
Experimental Results: Significantly inhibited B16F10 tumor growth.

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Animal/Disease Models:C57BL/6J (8–12 weeks old, no specific pathogen; wild-type and Nlrp3-/-)[1]
Doses: 20 mg/kg
Route of Administration: Intraperitoneal injection; every other day
Experimental Results: In wild-type mice, tumor IL-1β levels increased to approximately 4000 pg/mL/100 mg (n=5), IL-18 levels increased to approximately 1800 pg/mL/100 mg (n=5), and the proportion of caspase-1+ macrophages increased to 26.9% (n=5); these effects disappeared in Nlrp3-/- mice. On day 26, tumor volume decreased to approximately 200 mm3 (n=5) and tumor weight decreased to approximately 0.5 g (n=5) in wild-type mice; such effects were not observed in Nlrp3-/- mice. In wild-type mice, the tumor-infiltrating CD4+ T cell count increased to approximately 25 × 10⁵ (n=5), the CD8+ T cell count increased to approximately 20 × 10⁵ (n=5), and the percentage of IFN-γ+ CD8+ T cells increased to 22.9% (n=5); these effects were not observed in Nlrp3-/- mice.

[1]. A small molecule directly targets NLRP3 to promote inflammasome activation and antitumor immunity. Cell Death Dis. 2025;16(1):252. Published 2025 Apr 4.

[2]. A novel Hv1 inhibitor reveals a new mechanism of inhibition of a voltage-sensing domain. J Gen Physiol. 2021;153(9):e202012833.

C8H9N5

175.19

5418-95-1

White to light yellow solid

N/C(N)=N/C1=NC2=CC=CC=C2N1

2GBI

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: 本产品在运输和储存过程中需避光（避免光照）。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~250 mg/mL (~1427.02 mM; with sonication)

Solubility in Formulation 1: ≥ 2.08 mg/mL (11.87 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (20.8 mg/mL) to 400 μL of PEG300 and mix well; then add 50 μL of Tween-80 and mix well; finally add 450 μL of physiological saline and adjust the volume to 1 mL. Preparation of physiological saline: Dissolve 0.9 g of sodium chloride in double-distilled water and dilute to 100 mL to obtain clear physiological saline.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (11.87 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (20.8 mg/mL) to 900 μL of 20% SBE-β-CD saline and mix well. Preparation of 20% SBE-β-CD saline (4°C, store for one week): Dissolve 2 g of SBE-β-CD powder in 10 mL of saline until completely dissolved and clear.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)