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Beijing Tide Pharmaceutical Co., Ltd.
  • Founded in:

    1995-05-29
  • Country:

    China China
  • Address:

    No. 8 Rongjing East Street, Beijing Economic and Technological Development Zone, Beijing
  • Tax NO.:

    911103026000314683
  • Registered Funds:

    500 million yuan
  • Website:

  • Email:

Related Drugs
Ozagrel Sodium Injection
Ozagrel sodium. Excipients: glycine, citric acid, sodium chloride, sodium oxychloride.
Name Description Content CAS NO. Registered Holders
Ozagrel sodium

This product is a thromboxane (TX) synthase inhibitor, which can inhibit the generation of thromboxane A2 (TXA2) from prostaglandin H2 (PGH2), and promote the transfer of PGH2 derived from platelets to endothelial cells. Endothelial cells are used to synthesize PGI2, thereby improving the abnormal balance between TXA2 and prostaglandin PGI2. Theoretically, it can inhibit platelet aggregation and vasodilation. This product can improve movement disorders in the acute stage of cerebral thrombosis, improve circulatory disorders in the acute stage of cerebral ischemia, and improve abnormal energy metabolism during cerebral ischemia. Animal experiments have shown that intravenous administration can reduce plasma TXB2 levels, increase the ratio of 6-Keto-PGF1a/TXB2, inhibit platelet aggregation caused by different inducers, and prevent cerebral infarction caused by middle cerebral artery occlusion in rats. The half-maximal inhibitory concentration IC50 of this product for human platelet aggregation is low, at 4nM. Experiments using autologous blood injected into the subarachnoid hemorrhage model showed that continuous intravenous injection of this product has the effects of inhibiting blood TXB2 concentration and cerebral vasoconstriction.

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This product is a thromboxane (TX) synthase inhibitor, which can inhibit the generation of thromboxane A2 (TXA2) from prostaglandin H2 (PGH2), and promote the transfer of PGH2 derived from platelets to endothelial cells. Endothelial cells are used to synthesize PGI2, thereby improving the abnormal balance between TXA2 and prostaglandin PGI2. Theoretically, it can inhibit platelet aggregation and vasodilation. This product can improve movement disorders in the acute stage of cerebral thrombosis, improve circulatory disorders in the acute stage of cerebral ischemia, and improve abnormal energy metabolism during cerebral ischemia. Animal experiments have shown that intravenous administration can reduce plasma TXB2 levels, increase the ratio of 6-Keto-PGF1a/TXB2, inhibit platelet aggregation caused by different inducers, and prevent cerebral infarction caused by middle cerebral artery occlusion in rats. The half-maximal inhibitory concentration IC50 of this product for human platelet aggregation is low, at 4nM. Experiments using autologous blood injected into the subarachnoid hemorrhage model showed that continuous intravenous injection of this product has the effects of inhibiting blood TXB2 concentration and cerebral vasoconstriction.

189224-26-8 10
Pronase Granules
The main component of this product is pronase, which is a proteolytic enzyme produced by Streptomyces Griseus.
Name Description Content CAS NO. Registered Holders
EC 3.4.24.4

It is a proteolytic enzyme produced by Streptomyces Griseus

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It is a proteolytic enzyme produced by Streptomyces Griseus

9036-06-0 0
Flurbiprofen gel patch
The main ingredient of this product is flurbiprofen. Chemical structure: (±)-2-(2-fluoro-4-biphenyl)-propionic acid. Molecular formula: C15H13FO2 Molecular weight: 244.26
Name Description Content CAS NO. Registered Holders
Flurbiprofen

It has excellent analgesic and anti-inflammatory effects on pain, acute inflammation and chronic inflammation. 1. Analgesic effect: It has a strong inhibitory effect on the pain response caused by the Randall-Selitto method (rats) and uric acid synovitis (dogs). 2. Anti-inflammatory effect: (1) Effect on acute inflammation: It has a strong inhibitory effect on foot edema caused by carrageenan (rats), back edema caused by anti-rat rabbit serum (rats), ultraviolet erythema (guinea pigs), etc., and the effect is equivalent to or stronger than 1% indomethacin ointment, epinephrine ointment and methyl salicylate patch. (2) Effect on chronic inflammation: It has a strong inhibitory effect on granulation formation caused by formalin impregnated filter paper method (rats), adjuvant arthritis (rats), etc., and the effect is equivalent to or stronger than 1% indomethacin ointment, epinephrine ointment and methyl salicylate patch.

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It has excellent analgesic and anti-inflammatory effects on pain, acute inflammation and chronic inflammation. 1. Analgesic effect: It has a strong inhibitory effect on the pain response caused by the Randall-Selitto method (rats) and uric acid synovitis (dogs). 2. Anti-inflammatory effect: (1) Effect on acute inflammation: It has a strong inhibitory effect on foot edema caused by carrageenan (rats), back edema caused by anti-rat rabbit serum (rats), ultraviolet erythema (guinea pigs), etc., and the effect is equivalent to or stronger than 1% indomethacin ointment, epinephrine ointment and methyl salicylate patch. (2) Effect on chronic inflammation: It has a strong inhibitory effect on granulation formation caused by formalin impregnated filter paper method (rats), adjuvant arthritis (rats), etc., and the effect is equivalent to or stronger than 1% indomethacin ointment, epinephrine ointment and methyl salicylate patch.

5104-49-4 29
Esmolol Hydrochloride Injection
Main ingredients and chemical name: 4-(3-isopropylamino-2-hydroxypropoxy)phenylpropanoic acid methyl ester hydrochloride Molecular formula: C16H25NO4HCl Molecular weight: 331.84
Name Description Content CAS NO. Registered Holders
Esmolol hydrochloride

A selective β1-adrenergic receptor blocker with rapid onset and short duration of action. It mainly acts on the β1-adrenergic receptors of the myocardium. In large doses, it also has a blocking effect on the β2-adrenergic receptors of tracheal and vascular smooth muscle. It has no intrinsic sympathomimetic or membrane-stabilizing effects. It can reduce the heart rate of normal people during exercise and rest, and counteract the increase in heart rate caused by isoproterenol. The antihypertensive effect is correlated with the degree of β-adrenergic receptor blockade. The β-adrenergic receptor blocking effect basically disappears 10 to 20 minutes after the intravenous injection is stopped. It has typical β-adrenergic receptor blocker effects: reducing heart rate, reducing sinoatrial node automaticity, prolonging sinoatrial node recovery time, prolonging the AH interval during sinus rhythm and atrial rhythm, and prolonging the forward Wenckebach conduction cycle.

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A selective β1-adrenergic receptor blocker with rapid onset and short duration of action. It mainly acts on the β1-adrenergic receptors of the myocardium. In large doses, it also has a blocking effect on the β2-adrenergic receptors of tracheal and vascular smooth muscle. It has no intrinsic sympathomimetic or membrane-stabilizing effects. It can reduce the heart rate of normal people during exercise and rest, and counteract the increase in heart rate caused by isoproterenol. The antihypertensive effect is correlated with the degree of β-adrenergic receptor blockade. The β-adrenergic receptor blocking effect basically disappears 10 to 20 minutes after the intravenous injection is stopped. It has typical β-adrenergic receptor blocker effects: reducing heart rate, reducing sinoatrial node automaticity, prolonging sinoatrial node recovery time, prolonging the AH interval during sinus rhythm and atrial rhythm, and prolonging the forward Wenckebach conduction cycle.

81161-17-3 21
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