Trapidil

Trapidil inhibits the CD40/CD40L pathway of human monocytes and macrophages, reducing production of the proinflammatory cytokines TNF-α, IL-6, and IL-12^[2].
Trapidil increases intracellular cyclic adenosine monophosphate in human neutrophilic granulocytes, inhibiting their adherence, phagocytosis, and migration^[2].
Trapidil inhibits arachidonic acid liberation and thromboxane formation in thrombin-stimulated human platelets^[2].
Trapidil directly stimulates prostacyclin generation from arterial wall endothelial cells^[2].
Trapidil inhibits human mesangial cell proliferation in vitro via competitive antagonism of PDGF-BB binding to its surface receptors and modulation of β-receptor transcription^[7].
Trapidil decreases collagen synthesis in intimal cells cultured from human atherosclerotic plaques^[8].
Trapidil enhances cAMP levels and reduces cGMP levels in intimal cells cultured from human atherosclerotic plaques^[8].
Trapidil inhibits arachidonic acid- and U46619-induced platelet aggregation in human platelet-rich plasma with IC₅₀ values of 147 μM and 150 μM, respectively^[8].
Trapidil inhibits thromboxane B₂ formation in intact human platelets with an IC₅₀ of 224 μmol/L^[8].
Trapidil (10-100 μg/mL; 8 to 14 days) dose-dependently inhibits proliferation of low-passage human benign meningioma cells in vitro, with maximum inhibition (16% to 54% decrease) at 100 μg/mL, while 1 μg/mL trapidil has no significant effect after 8 to 14 days of treatment^[9].
Trapidil (10-100 μg/mL; 24 h total incubation) dose-dependently inhibits basal DNA synthesis in 3 of 7 low-passage human meningioma cell cultures in vitro, with maximum inhibition (36% to 53% decrease) at 100 μg/mL^[9].
Trapidil (100 μg/mL; 14 days) almost completely abolishes EGF-stimulated proliferation of human pituitary adenoma-derived fibroblasts in vitro, with no effect on basal proliferation^[9].
Trapidil (10-100 μM; 18 h) inhibits procoagulant activity induction in human peripheral blood mononuclear cells during allo-MLR, with significant inhibition at 10 μM and near-complete inhibition at 100 μM after 18 h of incubation^[11].
Trapidil (100 μM; 18 h) inhibits allo-MLR-induced tissue factor and CD40 expression on human monocytes, as well as allo-MLR-induced MCP-1 and MMP-9 production by human peripheral blood mononuclear cells^[11].
Trapidil (100 μM; 1 day) reduces CD40 expression on isolated human CD14⁺ monocytes stimulated with interferon-γ plus GM-CSF^[11].
Trapidil (3-100 μM; 1 day priming + 18 h co-culture) inhibits interferon-γ and CD154-induced MCP-1 production in human monocytic leukemia THP-1 cells with an IC₅₀ of 13.6 μM, when present during interferon-γ priming^[11].
Trapidil (10-100 μg/mL; 2-6 days) potently inhibits PDGF-dependent U251MG glioma cell proliferation (reducing growth to 46% of control at 100 μg/mL after 4 days) but has minimal effect on PDGF-independent U105MG glioma cells, and enhances the antiproliferative effect of ACNU on U251MG cells^[12].
Trapidil inhibits PDGF-induced proliferation of BALB/c 3T3 fibroblasts^[13].
Trapidil (400 μg/mL; 3 h) inhibits PDGF-stimulated migration of rat aortic VSMCs to 20 ± 2% of PDGF-only levels, with residual inhibitory activity retained even after PKA inhibition, and equivalent antimigratory activity to forskolin when both PKA and ROCK are inhibited^[15].
Trapidil (400 μg/mL; 1 h) completely inhibits PDGF-stimulated RhoA activation in rat aortic VSMCs^[15].
Trapidil (400 μg/mL; 16 h) completely inhibits PDGF-stimulated RhoA translocation from the soluble to the particulate fraction in rat aortic VSMCs^[15].
Trapidil (1-100 μM; 2 min preincubation, then 10 min PDGF-BB stimulation) concentration-dependently inhibits PDGF-BB-, PMA-, thrombin-, and LPS-induced MAP kinase phosphorylation in bovine coronary artery smooth muscle cells^[16].
Trapidil (1-100 μM; preincubation prior to 10-min PDGF-BB stimulation) concentration-dependently inhibits PDGF-BB-induced Raf-1 kinase activity in bovine coronary artery smooth muscle cells, with significant inhibition at 100 μM^[16].
Trapidil (0.1-100 μM; 10 min) concentration-dependently stimulates PKA activity in bovine coronary artery smooth muscle cells, with significant effects at 10 and 100 μM, reaching a maximal effect comparable to 10 nM PGE₁^[16].
Trapidil (5-500 μM; 16 h) dose-dependently reduces S-phase distribution and mitotic activity (S+G₂/M phase) in serum-stimulated primary cultured rat aortic VSMCs, with 500 μM producing the largest reductions of 58.6% and 49.6% respectively, but has no effect on cell cycle in quiescent, non-serum-stimulated VSMCs^[17].
Trapidil (5-500 μM; 10 min) inhibits serum-stimulated MAPK activity in primary cultured rat aortic VSMCs at 50 μM (59.3% inhibition) and 500 μM (80.9% inhibition) after 10 min of treatment, and also reduces basal MAPK activity by 72.0% at 500 μM in quiescent VSMCs^[17].
Trapidil (400 μg/mL; 18 h) increases PDGF β-receptor protein levels by 28±8% in rat aortic vascular smooth muscle cells^[18].
Trapidil (400 μg/mL; 18 h) increases MAP kinase phosphatase-1 protein expression by approximately 40% in rat aortic vascular smooth muscle cells^[18].
Trapidil (200-800 μg/mL; 30 min) does not affect in vitro PDGF β-receptor tyrosine kinase activity in preparations from rat aortic vascular smooth muscle cells^[18].
Trapidil (400 μg/mL; 18 h pre-incubation, 10 min PDGF stimulation) does not affect PDGF-stimulated tyrosine phosphorylation or protein levels of PLCγ, Ras GAP, PI3K p85 subunit, or Shc in rat aortic vascular smooth muscle cells^[18].
Trapidil (400 μg/mL; 18 h pre-incubation, 10 min/6 h PDGF stimulation) inhibits PDGF-stimulated MAP kinase activity by 35±7% at 10 minutes and 32% at 6 hours, and attenuates PDGF-induced Raf-1 hyperphosphorylation in rat aortic vascular smooth muscle cells^[18].
Trapidil (400 μg/mL; 18 h pre-incubation, 10 min/6 h PDGF stimulation) increases baseline cellular cAMP generation by 1.9-fold in rat aortic vascular smooth muscle cells, with cAMP levels remaining 1.3- to 1.5-fold higher than controls after PDGF stimulation for 10 minutes or 6 hours^[18].
Trapidil (50-400 μM; 2-14 days) dose-dependently promotes osteogenic differentiation of primary mouse calvarial osteoblast precursors without reducing cell viability, with maximal effects observed at 400 μM^[20].
Trapidil (50-400 μM; 5 min-24 h) activates BMP receptor signaling in primary mouse calvarial osteoblast precursors, which is required for its pro-osteogenic effects, as demonstrated by increased Smad1/5/9 phosphorylation, Id1 expression, and Id1 promoter activity^[20].
Trapidil (400 μM; 5 min-14 days) requires ALK3 to activate BMP signaling and promote osteogenic differentiation of primary mouse calvarial osteoblast precursors, as trapidil's effects are abolished by ALK3 depletion^[20].
Trapidil (400 μM; 5 min-14 days) requires autocrine BMP signaling to activate BMP receptors and promote osteogenic differentiation of primary mouse calvarial osteoblast precursors, and exhibits a synergistic pro-osteogenic effect with exogenous BMP2^[20].
Trapidil (50 μM, 200 μM, 400 μM; 2 days, 3 days, 14 days) dose-dependently promotes osteogenic differentiation of primary mouse calvarial osteoblast precursors, with 400 μM trapidil increasing ALP activity to 370 nmol/μg/min at 3 days and Tnap mRNA expression to 3.5-fold at 2 days, without affecting cell viability^[21].
Trapidil (50-400 μM; 4 days) dose-dependently inhibits RANKL + M-CSF-induced osteoclast formation in mouse bone marrow-derived macrophages, with no associated cellular toxicity^[22].
Trapidil (400 μM; 1 h pre-incubation) specifically inhibits RANKL-induced CREB activation, without affecting MAPK, Akt, or NF-κB pathways, in mouse bone marrow-derived macrophages^[22].
Trapidil (400 μM; 1 or 2 days) inhibits RANKL-induced NFATc1 mRNA and protein expression, without altering c-Fos expression, in mouse bone marrow-derived macrophages^[22].
Trapidil (12.5-200 μM; 48 h) enhances the viability of HG-treated primary NMCMs, with the optimal protective effect observed at 50 μM after 48 h of treatment^[23].
Trapidil (50 μM; 48 h) inhibits pyroptosis in HG-treated primary NMCMs when administered at 50 μM for 48 h^[23].
Trapidil (50 μM; 48 h) inhibits oxidative stress, reduces ROS levels, and restores mitochondrial membrane potential in HG-treated primary NMCMs when administered at 50 μM for 48 h^[23].
Trapidil (50 μM; 48 h) upregulates the GPX3/Nrf2 pathway by increasing GPX3 (protein and mRNA) and activated Nrf2 protein levels in HG-treated primary NMCMs when administered at 50 μM for 48 h^[23].
Trapidil (50 μM; 48 h)’s inhibitory effects on pyroptosis and oxidative stress, and its activating effect on Nrf2, are dependent on GPX3 in HG-treated primary NMCMs when administered at 50 μM for 48 h^[23].
Trapidil (48 h) increases PDGF β-receptor mRNA levels by approximately threefold in cultured mesangial cells^[24].
Trapidil attenuates PDGF-induced activation of extracellular signal-regulated protein kinases (ERKs) in cultured vascular smooth muscle cells^[24].
Trapidil (139 μM; 1 min) inhibits the secondary phase of ADP-induced aggregation of guinea-pig platelets with an IC₅₀ of 139 μM^[25].
Trapidil (146 μM; 1 min) inhibits ADP-induced ATP release from guinea-pig platelets with an IC₅₀ of 146 μM^[25].
Trapidil (251 μM; 1 min) inhibits arachidonic acid-induced aggregation of rabbit platelets with an IC₅₀ of 251 μM^[25].
Trapidil (121 μM; 1 min) inhibits arachidonic acid-induced ATP release from rabbit platelets with an IC₅₀ of 121 μM^[25].
Trapidil (226 μM; 1 min) inhibits thrombin-induced aggregation of washed rabbit platelets with an IC₅₀ of 226 μM^[25].
Trapidil (252 μM; 1 min) inhibits thrombin-induced ATP release from washed rabbit platelets with an IC₅₀ of 252 μM^[25].
Trapidil (203 μM; 1 min) inhibits TXA₂ mixture-induced aggregation of rat platelets with an IC₅₀ of 203 μM^[25].
Trapidil (150-1500 μM; 3 min) inhibits rabbit platelet thromboxane synthetase activity in a concentration-dependent manner, with 50% inhibition at 450 μM^[25].
Trapidil (122 μM; 30 min) inhibits low K_m phosphodiesterase activity in rabbit platelets with an IC₅₀ of 122 μM^[25].
Trapidil (100-400 μg/mL; 96 h) dose-dependently inhibits proliferation of primary human mesangial cells stimulated by FBS, PDGF-BB, bFGF, or EGF, with maximum 65.3% inhibition of PDGF-BB-stimulated proliferation at 100 μg/mL for 96 hours, and no cytotoxic effects at tested concentrations^[27].
Trapidil (100-400 μg/mL; 96 h) dose-dependently inhibits proliferation of NIH 3T3 fibroblasts stimulated by FBS, PDGF-BB, or bFGF, with the greatest effect on PDGF-BB-stimulated cells at tested concentrations for 96 hours^[27].
Trapidil (400-800 μg/mL; 2 h) competitively inhibits specific ¹²⁵I-PDGF-BB binding to primary human mesangial cells, with significant inhibition observed at 400 and 800 μg/mL during 2-hour coincubation at 4°C^[27].
Trapidil (400-800 μg/mL; 2 h) directly interacts with PDGF receptors on NIH 3T3 fibroblasts to inhibit specific ¹²⁵I-PDGF-BB binding, with significant inhibition observed at 400 and 800 μg/mL after 2-hour preincubation at 37°C^[27].
Trapidil (400 μg/mL; 48 h) induces a 150% increase in specific ¹²⁵I-PDGF-BB binding via receptor upregulation in primary human mesangial cells after 48-hour incubation at 37°C^[27].
Trapidil (400 μg/mL; 24-48 h) modulates PDGF β-receptor mRNA levels in primary human mesangial cells treated with 20 ng/mL PDGF-BB, causing a 30% decrease after 24 hours and a threefold increase after 48 hours^[27].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.