Tenidap sodium

Tenidap sodium selectively inhibits cytokine-stimulated SAA production without affecting HSA production in Hep 3B cells^[2].

Tenidap sodium suppresses IL-1, TNF, and IL-6 production in LPS-stimulated human PBMCs, with near-complete inhibition of IL-6^[2].
Tenidap sodium potently inhibits in vitro bone resorption induced by parathyroid hormone, vitamin D₃, IL-1α, TNF-α, and prostaglandin E₂^[2].

Tenidap sodium reduces LPS-induced IL-1 production and translational activity in GM-CSF-cultured human monocytes^[2].
Tenidap (5-10 μg/mL) sodium protects bovine and porcine cartilage from IL-1-induced catabolic effects and GAG loss and promotes cartilage repair^[2].
Tenidap (20 μg/mL) sodium reduces IL-1 receptor number and suppresses collagenase and stromelysin synthesis in human chondrocytes^[2].

Tenidap sodium inhibits leucocyte-endothelial cell adhesion in vitro across neutrophils, eosinophils, monocytes, and T cells^[2].

Tenidap sodium inhibits early monocyte differentiation markers in HL-60 cells, including CD14 expression and IFN-γ-stimulated C2 production^[2].

Tenidap sodium inhibits IL-1 synthesis and prostaglandin biosynthesis in LPS- and zymosan-stimulated mouse peritoneal macrophages^[2].

Tenidap sodium inhibits the cyclooxygenase pathway in rat basophilic leukemia cells and human peripheral polymorphonuclear leucocytes^[2].
Tenidap sodium inhibits COX-1, COX-2, and 5-LOX in rabbit peripheral venous blood samples, with COX-1 IC₅₀ 2.56 µM, COX-2 IC₅₀ 8.40 µM, and 5-LOX IC₅₀ 36.70 µM^[5].

Tenidap (0.5-100 µM; 5-10 min) sodium inhibits the db-cAMP/IBMX-stimulated [Cl⁻]_i increase in noncapacitated mouse sperm with an estimated IC₅₀ of 2.9 µM^[3].
Tenidap (0.5-100 µM; 60 min) sodium partially blocks capacitation-associated Em hyperpolarization in mouse sperm with an estimated IC₅₀ of 2.6 µM^[3].
Tenidap (0.5-100 µM; 10 min) sodium blocks ~50% of the HCO₃⁻-induced Em hyperpolarization in noncapacitated mouse sperm^[3].
Tenidap (0.5-100 µM; 60 min) sodium reduces the capacitation-associated pHi increase in mouse sperm with an estimated IC₅₀ of 3.5 µM^[3].
Tenidap (10 µM; 50 min) sodium is a potent opener of hKir2.3 stably expressed in CHO cells, increasing ⁸⁶Rb⁺ efflux with an EC₅₀ of 402 nM^[4].
Tenidap (10 µM; within seconds) sodium reversibly potentiates whole-cell hKir2.3 currents in CHO cells with an EC₅₀ of 1.3 µM^[4].
Tenidap (1-10 µM) sodium hyperpolarizes hKir2.3-expressing CHO cells and reduces input resistance at 10 µM^[4].
Tenidap (10-30 µM) sodium increases hKir2.3 currents in outside-out patches, and intracellular bovine serum albumin does not prevent potentiation, consistent with an extracellular site of action^[4].