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SML0071

Sigma-Aldrich

Trapidil

≥98% (HPLC)

Sinônimo(s):

AR 12008, Avantrin, N,N-diethyl-5-methyl-[1,2,4]Triazolo[1,5-a]pyrimidin-7-amine, Rocornal, Trapymin, Trapymine

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About This Item

Fórmula empírica (Notação de Hill):
C10H15N5
Número CAS:
15421-84-8
Peso molecular:
205.26
Número CE:
239-434-2
Número MDL:
MFCD00193104
Código UNSPSC:
41116107
ID de substância PubChem:
329825135
NACRES:
NA.77

Ensaio

≥98% (HPLC)

Formulário

powder

cor

white to tan

solubilidade

H2O: ≥15 mg/mL

temperatura de armazenamento

room temp

cadeia de caracteres SMILES

CCN(CC)c1cc(C)nc2ncnn12

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

chave InChI

GSNOZLZNQMLSKJ-UHFFFAOYSA-N

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Aplicação

Trapidil was used to study the mechanism of osteoclastogenesis and bone loss in mice.[1]

Ações bioquímicas/fisiológicas

Antiplatelet agent; competitive inhibitor of PDGF receptor; phosphodiesterase inhibitor, vasodilator
Trapidil is an antiplatelet agent that acts in part as a phosphodiesterase inhibitor and as a competitive inhibitor of the platelet-derived growth factor (PDGF) receptor. Trapidil, with its vasodilator and NO releasing effect may have some potential to diminish the tissue injury. Trapidil suppresses platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell (VSMC) proliferation by inhibiting Raf-1/extracellular signal-regulated kinase (ERK) via cAMP/protein kinase A (PKA). In addn. to cAMP/PKA activation, trapidil inhibits RhoA/ROCK activation.

Características e benefícios

This compound is a featured product for Cyclic Nucleotide research. Click here to discover more featured Cyclic Nucleotide products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Phosphodiesterases page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Pictogramas

Exclamation mark
GHS07

Palavra indicadora

Warning

Frases de perigo

H315,H319,H335

Classificações de perigo

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Órgãos-alvo

Respiratory system

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

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Certificados de análise (COA)

Lot/Batch Number
017M4754V
054M4740V
081M4709V

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Visite a Biblioteca de Documentos

Sun-Don Kim et al.
Biochemical pharmacology, 86(6), 782-790 (2013-08-10)
Trapidil, a platelet-derived growth factor antagonist, was originally developed as a vasodilator and anti-platelet agent and has been used to treat patients with ischemic coronary heart, liver, and kidney disease. In this study, we investigated the effects of trapidil on
Gaetano Ragno et al.
Analytical and bioanalytical chemistry, 389(3), 923-929 (2007-08-07)
A novel analytical technique able to determine the anti-ischemic drug trapidil in human serum and urine is proposed. In order to achieve satisfactory sensitivity and selectivity, an extraction procedure was required to isolate the drug from complex matrixes such as
W Sziegoleit et al.
International journal of clinical pharmacology and therapeutics, 45(1), 10-15 (2007-01-30)
In this study the effect of locally administered trapidil on human hand veins was examined. 10 healthy male volunteers aged 20 - 30 years were included. The dorsal hand vein compliance technique was used. In a crossover design the influence
Jodie M Dodd et al.
The Cochrane database of systematic reviews, (6)(6), CD006780-CD006780 (2010-06-18)
Pregnancy complications such as pre-eclampsia and eclampsia, intrauterine growth restriction and placental abruption are thought to have a common origin related to abnormalities in the development and function of the placenta. To compare, using the best available evidence, the benefits
Vasile Sirbu et al.
Journal of cardiovascular medicine (Hagerstown, Md.), 12(1), 55-58 (2010-11-04)
The use of drug-eluting stents (DES) allowed the reduction in the need for repeat revascularization. At the culprit site in acute myocardial infarction patients treated with first-generation DES, the interaction between the eluted drug and the underlying necrotic core may
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