MK 287
MK 287 is a potent, selective and orally active antagonist of platelet-activating factor receptor (PAFR). MK 287 can inhibit [3H]C18-PAF binding to human platelet, polymorphonuclear leukocyte (PMN) and lung membranes with K1 values of 6.1, 3.2, and 5.49 nM, respectively. MK 287 can inhibit PAF-induced aggregation of platelets in plasma or gel-filtered platelets and elastase release from PMNs with ED50 values of 56, 1.5 and 4.4 nM. MK 287 can be used for the research of cardiovascular disease, such as thrombosis.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- CAS No.: 135947-75-0
- 화학식: C25H34O9S
- 분자량:510.60
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
Chemical Information
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CAS No. 135947-75-0
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분자량 510.60
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화학식 C25H34O9S
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SMILES
CCCOC1=C(C=C([C@H]2O[C@H](C3=CC(OC)=C(C(OC)=C3)OC)CC2)C=C1OC)S(CCO)(=O)=O
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)