A repagermanium hydrolysate, 3-(trihydroxygermyl)propanoic acid (THGP), reduces pain and inflammation through unknown mechanisms. In the present study, we tested if THGP would directly react with H₂S, a gasotransmitter, because H₂S enhances Ca_v3.2 T-type Ca²⁺ channel activity by cancelling its zinc inhibition and nociceptor excitability. LC-MS/MS and ¹H-NMR analyses showed that THGP and Na₂S, an H₂S donor, when mixed, produced a compound containing a sulfur atom bound to the germanium atom, which was reduced by addition of ZnCl₂ in a concentration-dependent manner. THGP blocked the Na₂S-induced increase in low voltage-gated Ba²⁺ currents in Ca_v3.2-transfected HEK293 cells. Systemic administration of THGP blocked the intraplantar Na₂S-induced mechanical allodynia in mice. THGP also suppressed the burn injury-induced mechanical allodynia in the hindpaw and the bladder pain accompanying cyclophosphamide-induced cystitis in mice, which had upregulation of cystathionine-γ-lyase, an H₂S-forming enzyme, in the hindpaw and bladder tissues, respectively. Our data suggest that THGP suppresses H₂S-dependent enhancement of Ca_v3.2 activity and somatic or visceral pain by trapping sulfide.