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.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 99.92%
- CAS 番号: 162412-70-6
- 分子式: C28H25NaO9
- 分子量:528.48
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保管条件:
-20°C, protect from light, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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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
生物活性
製品説明
IC50 & Target
[1]|
ETA 0.17 μM (Ki) |
ETB 133.8 μM (Ki) |
体外実験
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 % |
体内実験
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.
化学情報
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CAS 番号 162412-70-6
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性状 Solid
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分子量 528.48
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
-20°C, protect from light, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
プロトコル
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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.
純度とドキュメンテーション
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データシート (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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取扱説明書 (2659 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
PD-156707 関連分類
HY-123744 関連分類
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