PD-156707
Based on 1 Customer Validation
PD-156707 is an orally active, nonpeptide and selective Endothelin-A receptor antagonist. PD-156707 binds to human ET-A and ET-B receptors with Ki values of 0.17 nM and 133.8 nM, respectively. PD-156707 shows reversal of established chronic hypoxic pulmonary hypertension in rats. PD-156707 can be used for the study of diseases associated with abnormal ET-A receptor activation, particularly pulmonary hypertension, stroke, and heart failure.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 99.92%
- CAS. Nr.: 162412-70-6
- Formel: C28H25NaO9
- Molecular Weight:528.48
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Speicherung:
-20°C, protect from light, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
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Endothelin 1 (swine, human) TFAEndothelin -
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BQ-788 sodium saltETB Receptor Antagonist
Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
ETA 0.17 μM (Ki) |
ETB 133.8 μM (Ki) |
In Vitro
PD-156707 inhibits inositol phosphate production induced by ET-1 in Ltk cells (IC50 = 2.4 nM) and arachidonic acid release stimulated by ET-1 in rabbit renal artery VSMC cells (IC50 = 1.1 nM)[1].
PD-156707 (0.1-10 μM) cause a rightward shift in the concentration-response curve of ET-1-stimulated contraction of rabbit femoral artery[1].
PD-156707 (1 μM) exerts a significant inhibitory effect on spontaneous neointimal proliferation of transverse sections of human saphenous vein[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Note | T1/2 | AUC | Cmax | Tmax | F |
|---|---|---|---|---|---|---|---|---|
| Dog[1] | 2.5 mg/kg | i.v. | / | 0.62 h | 1.5 μg·h/mL | / | / | / |
| Dog[1] | 5 mg/kg | p.o. | fasted | 1.2 h | 2.0 μg·h/mL | 1.52 mg/mL | 0.69 h | 67 % |
| Dog[1] | 5 mg/kg | p.o. | fet | 1.9 h | 0.59 μg·h/mL | 0.48 mg/mL | 2.5 h | 20 % |
| Monkey[1] | 10 mg/kg | i.v. | / | 1.19 h | 42.3 μg·h/mL | / | / | / |
| Monkey[1] | 10 mg/kg | p.o. | / | / | 23.5 μg·h/mL | 19.2 μg·h/mL | 0.833 h | 55 % |
| Rabbit[1] | 15 mg/kg | i.v. | / | 0.553 h | 29.3 μg·h/mL | / | / | / |
| Rat[1] | 10 mg/kg | i.v. | / | 1.75 h | 25.3 μg·h/mL | / | / | / |
| Rat[1] | 10 mg/kg | p.o. | / | 3.76 h | 13.9 μg·h/mL | 12.6 mg/mL | 0.25 h | 54.9 % |
| Rat[1] | 15 mg/kg | p.o. | / | 1.93 h | 5.55 μg·h/mL | 0.985 mg/mL | 4.0 h | 18.9 % |
In Vivo
PD-156707 (0.003-0.3 mg/kg/h, i.v. infusion, 1 h) shows dose-dependent inhibition of ET-1-induced renal vascular resistance (RVR) increase in rabbits[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male New Zealand White rabbits (2-3 kg)[2]
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Dosage:0.003, 0.01, 0.03, 0.3 mg/kg/h
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Administration:i.v. infusion, 1 h
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Result:Showed dose-dependent inhibition of endothelin-1 (ET-1)-induced renal vascular resistance (RVR) increase.
Exerts no significant effect on baseline MAP, heart rate, RBF, or RVR.
Blocks ET-1-induced RVR increase without attenuating ET-1-induced MAP reduction.
Chemical Information
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CAS. Nr. 162412-70-6
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Appearance Solid
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Molecular Weight 528.48
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Formel C28H25NaO9
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Color White to off-white
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SMILES
O=C(/C(C1=CC=C2OCOC2=C1)=C(C(C3=CC=C(C=C3)OC)=O)/CC4=CC(OC)=C(C(OC)=C4)OC)O[Na]
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
-20°C, protect from light, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
Protokoll
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Reinheit & Dokumentation
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Data Sheet (278 KB)
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SDS (398 KB)
- English - EN (398 KB)
- Français - FR (398 KB)
- Deutsch - DE (398 KB)
- Norwegian - NO (398 KB)
- Español - ES (398 KB)
- Swedish - SV (398 KB)
- Italian - IT (398 KB)
- Korean - KR (398 KB)
- Portuguese - PT (398 KB)
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Handling Instructions (2659 KB)
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
PD-156707 Related Classifications
HY-123744 Related Classifications
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