| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
|
||
| 10mg |
|
||
| 25mg |
|
||
| 50mg |
|
||
| 100mg |
|
||
| 250mg |
|
||
| Other Sizes |
Purity: ≥98%
| Targets |
PDGF
|
|---|---|
| ln Vitro |
Trapidil breaks the autocrine loop by acting on PDGF and PDGF receptors.Significant antiproliferative activity has been demonstrated by tramadil[1]. The addition of 100–400 μg/ml trapidil significantly inhibited the growth of cells stimulated by various growth factors (FCS, PDGF-BB, bFGF, and EGF), with PDGF-BB stimulating Mesangial cell (MC) growth being most inhibited. The medication had a dose-dependent, presumably targeted effect. ADP, arachidonic acid, PAF, collagen, calcium ionophore, and other aggregating agents are all targets of the anti-platelet medication tramadil. It works by inhibiting thromboxane A2 biosynthesis, counteracting its effects at the receptor level, and promoting prostacyclin synthesis and release[2]. In co-cultures of bone marrow cells and osteoblasts, tratidil significantly reduced the formation of osteoclasts while having no effect on the expression of osteoprotegerin or receptor activator of NF-κB ligand (RANKL) in osteoblasts. Furthermore, trapidil inhibited the formation of osteoclasts from osteoclast precursors induced by RANKL. Without influencing the expression of c-Fos, which serves as a crucial upstream activator of NFATc1 during osteoclastogenesis, tramadil decreased the RANKL-induced expression of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), a master transcription factor for osteoclastogenesis. Moreover, it has been documented that rivatimil activates protein kinase A and inhibits phosphodiesterase, thromboxane A2, and CD40 signaling[3].
|
| ln Vivo |
Trapidil is an antiplatelet medication that specifically antagonizes platelet-derived growth factors and has antiproliferative effects following balloon angioplasty in rat and rabbit models[1]. In an animal model of interleukin-1-induced osteoclast formation and bone resorption, tramadil demonstrated a strong inhibitory effect. Following intraperitoneal injections of trapidil, no abnormal symptoms, including weight changes, diarrhea, elevated fever, and convulsions, were noted[3].
|
| Cell Assay |
The Trypan blue dye exclusion test and the LDH assay were used to assess cell viability. After being exposed to various mitogens and drugs, cells were seeded in serum-free medium. The cells' supernatants were obtained, centrifuged, and the concentration of LDH was measured. As a positive control, supernatants from cells that had been sonicated were employed. In order to completely rule out Trapidil having a cytotoxic effect on human MC, cells that had been cultured for four days both with and without the medication were challenged with new medium containing 10% FBS, and the rate of cell division was assessed.
|
| Animal Protocol |
ICR mice
5 or 20 mg/kg i.p. |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
The time to peak concentration (Tmax) of tropidil is 1 hour. The apparent clearance after a single dose is 179 mL/min, and the apparent clearance after steady-state administration is 273 mL/min. Biological Half-Life The elimination half-life after a single dose is 1.31 hours, and the elimination half-life after steady-state administration is 1.14 hours. |
| References | |
| Additional Infomation |
Trapidil belongs to the triazolopyrimidine class of drugs. Trapidil is a platelet-derived growth factor antagonist, initially developed as a vasodilator and antiplatelet drug for the treatment of patients with ischemic coronary artery disease, liver disease, and kidney disease. It is a coronary vasodilator. Drug Indications: Used to treat chronic stable angina. Mechanism of Action: Trapidil is believed to inhibit cyclic adenosine monophosphate (cAMP) phosphodiesterase. The resulting increase in cAMP levels enhances the inhibitory effect of adenosine on platelets. Decreased platelet activation may be the reason why Trapidil reduces thromboxane A2 production. Increased cAMP levels may also be the reason for Trapidil's vasodilatory effect. Increased cAMP in the heart activates L-type calcium channels, leading to enhanced protein kinase A (PKA) activity, which in turn causes enhanced depolarization and positive inotropic effects. Furthermore, PKA inactivates Raf-1, the activator of mitogen-activated protein kinase (MAPK), thereby reducing MAPK activation. The reduction in MAPK inhibits the binding of PDGF to its receptor, thus preventing cell division.
Pharmacodynamics Trapidil has vasodilatory and antiplatelet aggregation effects and can inhibit the activity of platelet-derived growth factor (PDGF). |
| Molecular Formula |
C10H15N5
|
|---|---|
| Molecular Weight |
205.2596
|
| Exact Mass |
205.132
|
| Elemental Analysis |
C, 58.51; H, 7.37; N, 34.12
|
| CAS # |
15421-84-8
|
| Related CAS # |
15421-84-8
|
| PubChem CID |
5531
|
| Appearance |
White to off-white solid powder
|
| Density |
1.2±0.1 g/cm3
|
| Melting Point |
98-99.4° (Pfeifer); 102-104° from heptane (Tenor)
|
| Index of Refraction |
1.626
|
| LogP |
1.45
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
3
|
| Heavy Atom Count |
15
|
| Complexity |
206
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
N(C([H])([H])C([H])([H])[H])(C([H])([H])C([H])([H])[H])C1=C([H])C(C([H])([H])[H])=NC2=NC([H])=NN12
|
| InChi Key |
GSNOZLZNQMLSKJ-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C10H15N5/c1-4-14(5-2)9-6-8(3)13-10-11-7-12-15(9)10/h6-7H,4-5H2,1-3H3
|
| Chemical Name |
N,N-diethyl-5-methyl-[1,2,4]triazolo[1,5-a]pyrimidin-7-amine
|
| Synonyms |
AR 12008; AR-12008; AR12008
|
| HS Tariff Code |
2934.99.03.00
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO: ~41 mg/mL (~199.8 mM)
Ethanol: ~41 mg/mL (~199.8 mM) Water: ~41 mg/mL (~199.8 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (487.19 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.8719 mL | 24.3593 mL | 48.7187 mL | |
| 5 mM | 0.9744 mL | 4.8719 mL | 9.7437 mL | |
| 10 mM | 0.4872 mL | 2.4359 mL | 4.8719 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
COA