A selective beta-1-adrenergic receptor blocker with no intrinsic sympathomimetic activity and membrane stabilizing effect. Its affinity for beta-1-receptors is 11 to 34 times greater than that for beta-2-receptors. Its selectivity for beta-1 receptors is 4 times that of atenolol. It has a long duration of action (more than 24 hours). Continuous use can control symptoms well without tolerance. It has minimal side effects on the respiratory system and has no effect on fat metabolism.

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. It antagonizes the effects of opioids by competing for the same receptor sites.

This product is an opioid receptor antagonist, which has almost no pharmacological activity itself, but can competitively antagonize various opioid receptors and has a strong affinity for m receptors. It can completely or partially correct the central inhibitory effects of opioid substances, such as respiratory depression, sedation and hypotension; it has a wake-up effect on animals with acute ethanol poisoning; it is a pure opioid receptor antagonist and does not cause respiratory depression, psychotomimetic reactions or miotic reactions; there is no drug resistance, nor physiological or mental dependence.

This product is an opioid receptor antagonist, which has almost no pharmacological activity itself, but can competitively antagonize various opioid receptors and has a strong affinity for m receptors. It can completely or partially correct the central inhibitory effects of opioid substances, such as respiratory depression, sedation and hypotension; it has a wake-up effect on animals with acute ethanol poisoning; it is a pure opioid receptor antagonist and does not cause respiratory depression, psychotomimetic reactions or miotic reactions; there is no drug resistance, nor physiological or mental dependence.

This product is an opioid receptor antagonist, which has almost no pharmacological activity itself, but can competitively antagonize various opioid receptors and has a strong affinity for m receptors. It can completely or partially correct the central inhibitory effects of opioid substances, such as respiratory depression, sedation and hypotension; it has a wake-up effect on animals with acute ethanol poisoning; it is a pure opioid receptor antagonist and does not cause respiratory depression, psychotomimetic reactions or miotic reactions; there is no drug resistance, nor physiological or mental dependence.

This product is an opioid receptor antagonist. It has almost no pharmacological activity itself, but it can competitively antagonize various opioid receptors and has a strong affinity for m receptors. (I) Pharmacological action 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 acute ethanol poisoning in animals. 3. It is a pure opioid receptor antagonist, that is, it does not have the "excitability" or morphine-like effects of other opioid receptor antagonists; it does not cause respiratory depression, psychotomimetic reactions or pupil constriction reactions. 4. No drug resistance is observed, nor is there any physiological or mental dependence. 5. Although the mechanism of action is not yet fully understood, there is sufficient evidence to show that it antagonizes the effects of opioids by competing for the same receptor sites. (II) Clinical pharmacology In a clinical study organized by the Chinese Society of Neurosurgery and the Chinese Journal of Neurosurgery, 18 large hospitals across the country (including neurological specialty hospitals) conducted a double-blind randomized controlled clinical study on the treatment of acute craniocerebral injury with naloxone injection. A total of more than 500 cases were completed. The experimental group added this product to the basic treatment plan. The dosage was 0.3mg/kg/body weight/day. After diluting it to 500ml with normal saline or balanced solution, it was continuously dripped for 24 hours using an infusion pump. After 3 consecutive days of use, the dosage was uniformly reduced to 4.8mg/day, and the drug was stopped after 7 consecutive days. Results Compared with the placebo control group that did not add this product but only used basic treatment, the mortality rate of the experimental group was 12.5%, and that of the placebo control group was 17.3%. There was a significant difference between the two groups, and the GCS score, GOS score, language motor function and quality of life score of the experimental group were significantly better than those of the placebo group. During the treatment period, a total of 8 patients developed liver and kidney dysfunction to varying degrees after taking the medicine, but there was no evidence to prove that it was related to the medicine. (III) Toxicology 1. For single-dose intravenous administration, the LD50 of rats and mice is 150mg/kg and 109mg/kg respectively; for single-dose subcutaneous injection, the LD50 of newborn rats is 260mg/kg. 2. No animal experiments have been conducted to evaluate the carcinogenicity of this product. 3. Fertility experiments on mice and rats with 50 times the human dose of this product showed no impairment of fertility.

This product is an opioid receptor antagonist. It has almost no pharmacological activity itself, but it can competitively antagonize various opioid receptors and has a strong affinity for m receptors. (I) Pharmacological action 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 acute ethanol poisoning in animals. 3. It is a pure opioid receptor antagonist, that is, it does not have the "excitability" or morphine-like effects of other opioid receptor antagonists; it does not cause respiratory depression, psychotomimetic reactions or pupil constriction reactions. 4. No drug resistance is observed, nor is there any physiological or mental dependence. 5. Although the mechanism of action is not yet fully understood, there is sufficient evidence to show that it antagonizes the effects of opioids by competing for the same receptor sites. (II) Clinical pharmacology In a clinical study organized by the Chinese Society of Neurosurgery and the Chinese Journal of Neurosurgery, 18 large hospitals across the country (including neurological specialty hospitals) conducted a double-blind randomized controlled clinical study on the treatment of acute craniocerebral injury with naloxone injection. A total of more than 500 cases were completed. The experimental group added this product to the basic treatment plan. The dosage was 0.3mg/kg/body weight/day. After diluting it to 500ml with normal saline or balanced solution, it was continuously dripped for 24 hours using an infusion pump. After 3 consecutive days of use, the dosage was uniformly reduced to 4.8mg/day, and the drug was stopped after 7 consecutive days. Results Compared with the placebo control group that did not add this product but only used basic treatment, the mortality rate of the experimental group was 12.5%, and that of the placebo control group was 17.3%. There was a significant difference between the two groups, and the GCS score, GOS score, language motor function and quality of life score of the experimental group were significantly better than those of the placebo group. During the treatment period, a total of 8 patients developed liver and kidney dysfunction to varying degrees after taking the medicine, but there was no evidence to prove that it was related to the medicine. (III) Toxicology 1. For single-dose intravenous administration, the LD50 of rats and mice is 150mg/kg and 109mg/kg respectively; for single-dose subcutaneous injection, the LD50 of newborn rats is 260mg/kg. 2. No animal experiments have been conducted to evaluate the carcinogenicity of this product. 3. Fertility experiments on mice and rats with 50 times the human dose of this product showed no impairment of fertility.

This product is an opioid receptor antagonist. It has almost no pharmacological activity itself, but it can competitively antagonize various opioid receptors and has a strong affinity for m receptors. (I) Pharmacological action 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 acute ethanol poisoning in animals. 3. It is a pure opioid receptor antagonist, that is, it does not have the "excitability" or morphine-like effects of other opioid receptor antagonists; it does not cause respiratory depression, psychotomimetic reactions or pupil constriction reactions. 4. No drug resistance is observed, nor is there any physiological or mental dependence. 5. Although the mechanism of action is not yet fully understood, there is sufficient evidence to show that it antagonizes the effects of opioids by competing for the same receptor sites. (II) Clinical pharmacology In a clinical study organized by the Chinese Society of Neurosurgery and the Chinese Journal of Neurosurgery, 18 large hospitals across the country (including neurological specialty hospitals) conducted a double-blind randomized controlled clinical study on the treatment of acute craniocerebral injury with naloxone injection. A total of more than 500 cases were completed. The experimental group added this product to the basic treatment plan. The dosage was 0.3mg/kg/body weight/day. After diluting it to 500ml with normal saline or balanced solution, it was continuously dripped for 24 hours using an infusion pump. After 3 consecutive days of use, the dosage was uniformly reduced to 4.8mg/day, and the drug was stopped after 7 consecutive days. Results Compared with the placebo control group that did not add this product but only used basic treatment, the mortality rate of the experimental group was 12.5%, and that of the placebo control group was 17.3%. There was a significant difference between the two groups, and the GCS score, GOS score, language motor function and quality of life score of the experimental group were significantly better than those of the placebo group. During the treatment period, a total of 8 patients developed liver and kidney dysfunction to varying degrees after taking the medicine, but there was no evidence to prove that it was related to the medicine. (III) Toxicology 1. For single-dose intravenous administration, the LD50 of rats and mice is 150mg/kg and 109mg/kg respectively; for single-dose subcutaneous injection, the LD50 of newborn rats is 260mg/kg. 2. No animal experiments have been conducted to evaluate the carcinogenicity of this product. 3. Fertility experiments on mice and rats with 50 times the human dose of this product showed no impairment of fertility.