Trapidil

SKU: orb1310960

Description

Trapidil (Avantrin) is a small molecule originally developed as a coronary vasodilator and antiplatelet agent. It has been used in research models of ischemic disease, with studies investigating its effects on vascular tone and platelet aggregation in both in vitro and in vivo experimental systems.

Research Area

Cardiovascular Research, Metabolism Research, Signal Transduction

Key Properties

• CAS Number: 15421-84-8
• MW: 205.26
• Purity: 99.96% (May vary between batches)
• Formula: C₁₀H₁₅N₅
• SMILES: N(CC)(CC)C=1N2C(N=C(C)C1)=NC=N2
• Target: PDE,PDGFR
• Solubility: Ethanol:39 mg/mL (190 mM);H2O:38 mg/mL (185.13 mM);DMSO:39 mg/mL (190 mM)

Bioactivity

• In Vivo:
  Trapidil is an antiplatelet drug with specific platelet-derived growth factor antagonism and antiproliferative effects in the rat and rabbit models after balloon angioplasty. Trapidil had a potent inhibitory effect on osteoclast formation and bone resorption induced by interleukin-1 in an animal model. No abnormal symptoms, such as changes in body weight, diarrhea, high fever, and convulsion, were observed after intraperitoneal injections of trapidil.
• In Vitro:
  Trapidil interrupts the autocrine loop at the PDGF and PDGF-receptor level.Trapidil has proved to possess a significant antiproliferative activity. The addition of 100 to 400 μg/ml trapidil significantly reduced cell proliferation induced by different growth factors (FCS, PDGF-BB, bFGF, EGF), the highest inhibitory effect being on PDGF-BB stimulated Mesangial cell(MC) growth. The effect of the drug was dose-dependent and seemingly specific. Trapidil is an anti-platelet drug active against various aggregating agents, such as collagen, ADP, arachidonic acid, PAF and calcium ionophore. It exerts its action by blocking the biosynthesis of thromboxane A2 and antagonizing its effect at the receptor level, and by stimulating the synthesis and release of prostacyclin. Trapidil strongly inhibited osteoclast formation in co-cultures of bone marrow cells and osteoblasts without affecting receptor activator of NF-κB ligand (RANKL) or osteoprotegerin expression in osteoblasts. In addition, trapidil suppressed RANKL-induced osteoclast formation from osteoclast precursors. Trapidil reduced RANKL-induced expression of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), a master transcription factor for osteoclastogenesis, without affecting the expression of c-Fos that functions as a key upstream activator of NFATc1 during osteoclastogenesis. Trapidil has also been reported to inhibit phosphodiesterase, thromboxane A2, and CD40 signaling and activate protein kinase A.
• Cell Research:
  Cell viability was determined by Trypan blue dye exclusion test and LDH assay. Supernatants, collected from cells seeded in serum-free medium and exposed to the different mitogens and drugs tested, were centrifuged and LDH concentration determined. Supernatants obtained from sonicated cells were used as a positive control. Furthermore, to definitely exclude a cytotoxic effect of Trapidil on human MC, cells incubated for four days with and without the drug were challenged with fresh medium containing 10% FBS, and cell proliferation evaluated. (Only for Reference)

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

AR 12008, AR12008, AR-12008, Avantrin, Inhibitor, inhibit, Platelet-derived growth factor receptor, PDGFR, PDE, Trapidil, Trapymin, Trapymine, Rocornal

Compound Identifiers

PubChem CID

5531