NQ 301 - CAS 130089-98-4
Category: Inhibitor
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Molecular Weight:
NQ 301 is a CD45 inhibitor with IC50 value of 200 nM. It can block inflammation in a delayed-type hypersensitivity model in vivo.
≥98% by HPLC
NQ-301; NQ 301; NQ301. 2-[(4-Acetylphenyl)amino]-3-chloro-1,4-naphthalenedione
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1.Antiplatelet and antithrombotic activities of NQ301, 2-chloro-3-(4-acetophenyl)-amino-1,4-naphthoquinone.
Kang WS;Ryu CK;Chung KH;Ko MW;Joo JC;Yuk DY;Yoo HS;Yun YP Biol Pharm Bull. 1999 Dec;22(12):1284-7.
The antiplatelet and antithrombotic activities of a newly synthesized NQ301, 2-chloro-3-(4-acetophenyl)-amino-1,4-naphthoquinone, were investigated on human platelet aggregation in vitro and rats ex vivo, and murine pulmonary thrombosis in vivo. NQ301 potently inhibited ADP-, collagen-, epinephrine- and calcium ionophore A23187-induced human platelet aggregation in a concentration-dependent manner in vitro. NQ301 significantly inhibited platelet aggregation in orally administered rats ex vivo. NQ301 prevented death due to pulmonary thrombosis in mice dose-dependently in vivo. NQ301 also showed significant prolongation of tail bleeding time in conscious mice. However, NQ301 did not alter such coagulation parameters as activated partial thromboplastin time, prothrombin time, and thrombin time in human plasma. These results suggest that NQ301 may be a promising antithrombotic agent, and the antithrombotic activity of NQ301 may be due to antiplatelet aggregation activity but not to in vitro anticoagulation.
2.Antiplatelet effect of 2-chloro-3-(4-acetophenyl)-amino-1,4-naphthoquinone (NQ301): a possible mechanism through inhibition of intracellular Ca2+ mobilization.
Zhang YH;Chung KH;Ryu CK;Ko MH;Lee MK;Yun YP Biol Pharm Bull. 2001 Jun;24(6):618-22.
The effects of 2-chloro-3-(4-acetophenyl)-amino-1,4-naphthoquinone (NQ301), an antithrombotic agent, on aggregation, binding of fibrinogen to glycoprotein (GP)IIb/IIIa complex and intracellular signals were investigated using human platelets. NQ301 significantly inhibited the collagen-, thrombin-, arachidonic acid-, thapsigargin- and calcium ionophore A23187-induced aggregation of washed human platelets with IC50 values of 13.0+/-0.1, 11.2+/-0.5, 21.0+/-0.9, 3.8+/-0.1 and 46.2+/-0.8 microM, respectively. NQ301 also significantly inhibited FITC-conjugated fibrinogen binding to human platelet surface GPIIb/IIIa complex, but failed to inhibit the fibrinogen binding to purified GPIIb/IIIa complex. These data demonstrate that NQ301 inhibits platelet aggregation by suppression of the intracellular pathway, rather than by direct inhibition of fibrinogen-GPIIb/IIIa complex binding. NQ301 significantly inhibited the increase of cytosolic Ca2+ concentration and ATP secretion, and also significantly increased platelet cAMP levels in the activated platelets. These results suggest that the antiplatelet activity of NQ301 may be mediated by inhibition of cytosolic Ca2+ mobilization, enhancement of cAMP production and inhibition of ATP secretion in activated platelets.
3.Thromboxane A2 synthase inhibition and thromboxane A2 receptor blockade by 2-[(4-cyanophenyl)amino]-3-chloro-1,4-naphthalenedione (NQ-Y15) in rat platelets.
Chang TS;Kim HM;Lee KS;Khil LY;Mar WC;Ryu CK;Moon CK Biochem Pharmacol. 1997 Jul 15;54(2):259-68.
The effects of 2-[(4-acetylphenyl)amino]-3-chloro-1,4-naphthalenedione (NQ-Y15), a synthetic 1,4-naphthoquinone derivative, on platelet activity and its mechanism of action were investigated. NQ-Y15 caused a concentration-dependent inhibition of the aggregation induced by thrombin, collagen, arachidonic acid (AA), and A23187. The IC50 values of NQ-Y15 on thrombin (0.1 U/mL)-, collagen (10 microg/mL)-, AA (50 microM)-, and A23187 (2 microM)-induced aggregation were 36.2 +/- 1.5, 6.7 +/- 0.7, 35.4 +/- 1.7, and 93.1 +/- 1.4 microM, respectively. NQ-Y15 also inhibited thrombin-, collagen-, AA-, and A23187-stimulated serotonin secretion in a concentration-dependent manner. However, a high concentration (100 microM) of NQ-Y15 showed no significant inhibitory effect on ADP-induced primary aggregation, which is independent of thromboxane A2 (TXA2) production in rat platelets. In fura-2-loaded platelets, the elevation of intracellular free calcium concentration stimulated by AA, thrombin, and 4-bromo-A23187 was inhibited by NQ-Y15 in a concentration-dependent manner. The formation of TXA2 caused by AA, thrombin, and collagen was inhibited significantly by NQ-Y15. NQ-Y15 inhibited TXA2 synthase in intact rat platelets, since this agent reduced the conversion of prostaglandin (PG) H2 to TXA2.
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CAS 130089-98-4 NQ 301

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