Hainan Bikai Pharmaceutical Co., Ltd.
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Founded in:
1993-03-22 -
Country:
China -
Address:
No. 10, Yaogu 1st Road, Haikou National High-tech Industrial Development Zone, Hainan Province -
Tax NO.:
91460100284031692C -
Registered Funds:
20 million yuan -
Website:
-
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Naloxone hydrochloride dihydrate |
1. Completely or partially correct the central inhibitory effects of opioids, such as respiratory depression, sedation and hypotension. 2. It has a wake-promoting effect on animals with acute ethanol intoxication. 3. It is a pure opioid receptor antagonist and does not have the excitatory or morphine-like effects of other opioid receptor antagonists; it does not cause respiratory depression, psychotomimetic reactions or miotic reactions. 4. No drug tolerance, nor physiological or psychological dependence, has been observed. 5. Although the mechanism of action is not fully understood, there is sufficient evidence to show that it antagonizes the effects of opioids by competing for the same receptor sites.
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1. Completely or partially correct the central inhibitory effects of opioids, such as respiratory depression, sedation and hypotension. 2. It has a wake-promoting effect on animals with acute ethanol intoxication. 3. It is a pure opioid receptor antagonist and does not have the excitatory or morphine-like effects of other opioid receptor antagonists; it does not cause respiratory depression, psychotomimetic reactions or miotic reactions. 4. No drug tolerance, nor physiological or psychological dependence, has been observed. 5. Although the mechanism of action is not fully understood, there is sufficient evidence to show that it antagonizes the effects of opioids by competing for the same receptor sites. |
51481-60-8 | 12 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Naloxone hydrochloride dihydrate |
1. Completely or partially correct the central inhibitory effects of opioids, such as respiratory depression, sedation and hypotension; 2. It has a wake-promoting effect on animals with acute ethanol intoxication; 3. It is a pure opioid receptor antagonist and does not have the excitatory or morphine-like effects of other opioid receptor antagonists; 4. It does not cause respiratory depression, psychotomimetic reactions or miotic reactions; 5. There is no drug tolerance, nor physiological or psychological dependence; 6. It antagonizes the effects of opioids by competing for the same receptor sites.
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1. Completely or partially correct the central inhibitory effects of opioids, such as respiratory depression, sedation and hypotension; 2. It has a wake-promoting effect on animals with acute ethanol intoxication; 3. It is a pure opioid receptor antagonist and does not have the excitatory or morphine-like effects of other opioid receptor antagonists; 4. It does not cause respiratory depression, psychotomimetic reactions or miotic reactions; 5. There is no drug tolerance, nor physiological or psychological dependence; 6. It antagonizes the effects of opioids by competing for the same receptor sites. |
51481-60-8 | 12 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Acetylsalicylic acid |
①Analgesic effect: It is mainly through inhibiting the synthesis of prostaglandins and other substances that can make pain sensitive to mechanical or chemical stimulation (such as bradykinin, histamine), and it is a peripheral analgesic. However, the possibility of central analgesia (possibly acting on the hypothalamus) cannot be ruled out; ②Anti-inflammatory effect: The exact mechanism is still unclear. It may be due to the fact that this product acts on inflamed tissues and inhibits the synthesis of prostaglandins or other substances that can cause inflammatory reactions (such as histamine) to play an anti-inflammatory role. Inhibition of the release of lysosomal enzymes and leukocyte chemotaxis may also be related to it; ③Antipyretic effect: It may act on the hypothalamic thermoregulatory center to cause peripheral vasodilation, increased skin blood flow, sweating, and increased heat dissipation to play an antipyretic role. This central effect may be related to the inhibition of prostaglandin synthesis in the hypothalamus; ④Anti-rheumatic effect: The anti-rheumatic mechanism of this product, in addition to antipyretic and analgesic effects, is mainly anti-inflammatory; ⑤Inhibition of platelet aggregation: It works by inhibiting platelet cyclooxygenase and reducing the production of prostaglandins.
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①Analgesic effect: It is mainly through inhibiting the synthesis of prostaglandins and other substances that can make pain sensitive to mechanical or chemical stimulation (such as bradykinin, histamine), and it is a peripheral analgesic. However, the possibility of central analgesia (possibly acting on the hypothalamus) cannot be ruled out; ②Anti-inflammatory effect: The exact mechanism is still unclear. It may be due to the fact that this product acts on inflamed tissues and inhibits the synthesis of prostaglandins or other substances that can cause inflammatory reactions (such as histamine) to play an anti-inflammatory role. Inhibition of the release of lysosomal enzymes and leukocyte chemotaxis may also be related to it; ③Antipyretic effect: It may act on the hypothalamic thermoregulatory center to cause peripheral vasodilation, increased skin blood flow, sweating, and increased heat dissipation to play an antipyretic role. This central effect may be related to the inhibition of prostaglandin synthesis in the hypothalamus; ④Anti-rheumatic effect: The anti-rheumatic mechanism of this product, in addition to antipyretic and analgesic effects, is mainly anti-inflammatory; ⑤Inhibition of platelet aggregation: It works by inhibiting platelet cyclooxygenase and reducing the production of prostaglandins. |
50-78-2 | 35 |
| 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 |