Valsartan Capsules

Mechanism of action: The activator of the renin-angiotensin-aldosterone system (RAAS) is angiotensin II, which is formed by angiotensin I under the action of angiotensin converting enzyme (ACE). Angiotensin II binds to specific receptors on the cell membranes of various tissues. It has many physiological effects, including direct or indirect participation in blood pressure regulation. Angiotensin II is a powerful vasoconstrictor that can exert a direct pressor effect, promote sodium reabsorption, and stimulate aldosterone secretion. Valsartan is an orally effective specific angiotensin (AT) II receptor antagonist that selectively acts on the AT1 receptor subtype, which responds to the known effects of angiotensin II and produces all known effects. The AT2 receptor subtype is not related to cardiovascular effects. Valsartan does not have any partial agonist activity on the AT1 receptor. The affinity of valsartan for the AT1 receptor is 20,000 times stronger than that for the AT2 receptor. ACE converts angiotensin I into angiotensin II and degrades bradykinin. Angiotensin II receptor antagonist - valsartan has no inhibitory effect on ACE, does not cause retention of bradykinin or substance P, and therefore does not cause cough. Clinical trials comparing valsartan with ACE inhibitors have confirmed that the incidence of dry cough in the valsartan group (2.6%) was significantly lower than that in the ACE inhibitor group (7.9%) (P < 0.05). In a clinical trial of patients who had developed dry cough symptoms after receiving ACE inhibitor treatment, 19.5%, 19.0%, and 68.5% of patients in the valsartan group, diuretic group, and ACEI group had cough, respectively (P < 0.05). Valsartan has no effect on other hormone receptors or ion channels known to play an important role in cardiovascular regulation. Efficacy: Valsartan reduces elevated blood pressure without affecting heart rate. For most patients, a single oral dose produces a hypotensive effect within 2 hours, reaches a peak effect within 4-6 hours, and the hypotensive effect is maintained for more than 24 hours after taking the drug. The maximum antihypertensive effect is achieved after 2-4 weeks of treatment, and the effect is maintained during long-term treatment. Combination with thiazide diuretics can further significantly enhance the antihypertensive effect. Sudden termination of valsartan treatment does not cause hypertension rebound or other clinical adverse events. In multiple-dose studies in patients with hypertension, valsartan had no significant effect on total cholesterol, fasting triglycerides, fasting blood glucose and uric acid levels. Preclinical safety information In preclinical safety studies conducted on several animals, there was no manifestation of systemic or target organ toxicity except for fetal toxicity in rabbits. In rats given 600 mg/Kg of the drug in the last three months of pregnancy and during lactation, the survival rate of their offspring was slightly reduced and their development was slightly delayed (see Use in Pregnant and Lactating Women). The main preclinical safety study results are caused by the pharmacological effects of the drug and have no clinical significance. In mice and rats, there is no evidence of mutagenicity, chromosomal clastogenicity or carcinogenicity.

The active ingredient of this product is valsartan.

The contents of this product are white or off-white granules and powder.

Suitable for mild and moderate essential hypertension.

Recommended dose: 80 mg of this product, once a day. The dose has nothing to do with race, age, and gender. It can be taken with meals or on an empty stomach (see absorption). It is recommended to take the medicine at the same time every day (such as in the morning). The exact antihypertensive effect is achieved within 2 weeks of medication, and the maximum therapeutic effect is achieved after 4 weeks. If the antihypertensive effect is not satisfactory, the daily dose can be increased to 160 mg, or a diuretic can be added. Patients with renal insufficiency (severe renal failure see contraindications) and non-biliary, non-choledostatic liver insufficiency do not need to adjust the dose. Valsartan can be used in combination with other antihypertensive drugs.

In a placebo- and Diovan-controlled trial in 2,316 hypertensive patients, the overall incidence of adverse events (AEs) in the Diovan group was similar to that in the placebo group. In a 6-month open-label extension trial in 642 hypertensive patients treated with 320 mg valsartan, the overall incidence of adverse events was similar to that observed in the placebo-controlled trial. The table below shows the incidence of adverse reactions reported in 10 placebo-controlled trials, with patients taking valsartan 10-320 mg/day for up to 12 weeks. Of the 2,316 patients, 1,281 and 660 took 80 mg and 160 mg, respectively. The incidence of adverse reactions seen was not related to the dose and duration of medication, so adverse reactions occurring at various doses were combined for statistics. The incidence of adverse reactions was not related to gender, age, or race. All adverse reactions with an incidence rate (1%) are listed in the table below (regardless of whether they are related to the drug under study). This product also includes adverse drug reactions reported in patients with hypertension after marketing. The incidence is defined as follows: very common (ge; 1/10); common (ge; 1/100, 1/1000); uncommon (ge; 1/1000, 1/100); rare (ge; 1/10000, 1/1000); very rare (1/10000). Infections Common: Viral infections Uncommon: Upper respiratory tract infection, pharyngitis, sinusitis Very rare: Rhinitis Blood and lymphatic system disorders Common: Neutropenia Very rare: Thrombocytopenia Immune system disorders Very rare: Hypersensitivity reactions, including serum sickness Psychiatric disorders: Uncommon: Insomnia, decreased libido Ear and inner ear labyrinth disorders Uncommon: Vertigo Vascular disorders Very rare: Vasculitis Respiratory system, chest and mediastinal disorders Uncommon: Cough Gastrointestinal disorders Uncommon: Diarrhea, abdominal pain Skin and subcutaneous tissue Tissue disorders Very rare: rash, pruritus Musculoskeletal and connective tissue disorders Uncommon: back pain Very rare: arthralgia, myalgia Systemic disorders and administration site reactions Uncommon: fatigue, asthenia, edema Laboratory findings: In rare cases, valsartan causes a decrease in hemoglobin and hematocrit. In controlled clinical trials, 0.8% and 0.4% of patients in the valsartan treatment group had a significant decrease in hematocrit and hemoglobin (20%). In contrast, only 0.1% of patients in the placebo group had a decrease in hematocrit and hemoglobin. In controlled clinical trials, neutropenia was found in 1.9% of valsartan-treated patients and 1.6% of ACEI-treated patients. Serum creatinine, serum potassium, and total bilirubin were significantly increased in 0.8%, 4.4%, and 6% of the valsartan group, and in 1.6%, 6.4%, and 12.9% of the ACEI group, respectively. Occasionally, liver function indexes were elevated. No special monitoring of laboratory indicators is required for patients with essential hypertension receiving valsartan treatment.

Allergic to valsartan or any other excipients in this product. Pregnancy (see [Use in Pregnant and Lactating Women])

Precautions for children: There are no studies on the effectiveness and safety of this product for children and adolescents (under 18 years old). Precautions for pregnancy and lactation: Pregnancy: Given the mechanism of action of angiotensin II antagonists, harm to the fetus cannot be ruled out. There have been reports that intrauterine administration of angiotensin-converting enzyme inhibitors (a specific class of drugs that act on RAAS) during the second and third trimesters of pregnancy can cause damage to the developing fetus or lead to fetal death. In addition, retrospective data show that the use of angiotensin-converting enzyme inhibitors in the first trimester of pregnancy has a potential risk of congenital defects. There have been reports of spontaneous abortion, oligohydramnios, and neonatal renal insufficiency when pregnant women inadvertently take valsartan. Similar to other drugs that directly act on RAAS, pregnant women should not use this product (see contraindications). For women who may become pregnant, doctors should inform them of the potential risks of this type of drug during pregnancy when prescribing drugs that act on RAAS. If pregnancy is discovered during medication, valsartan should be discontinued as soon as possible. Lactation: It is not clear whether valsartan is excreted in human milk. Valsartan is excreted in the milk of lactating rats. Therefore, this product should not be used during lactation. Precautions for the elderly: Although the systemic exposure concentration of valsartan in the elderly is slightly higher than that in young people, it has no clinical significance.

No obvious drug interactions have been found clinically. The following drugs have been studied: cimetidine, warfarin, furosemide, digoxin, atenolol, indomethacin, hydrochlorothiazide, amlodipine, and glibenclamide. Since valsartan is almost not metabolized, no clinical interaction has been found between related drugs and drugs that induce or inhibit the cytochrome P450 system. Although valsartan is mostly bound to plasma proteins, in vitro experiments have not found that it interacts with other plasma protein-bound drugs (such as diclofenac, furosemide, and warfarin) at this level. When combined with potassium-sparing diuretics (such as spironolactone, triamterene, and amiloride), potassium supplementation or the use of potassium-containing preparations can lead to increased blood potassium concentrations. Therefore, special attention should be paid when using drugs in combination.

Light-proof seal.

80mg

36 months.

TC Pharmaceuticals (Jiangsu) Co., Ltd.

• Founded in:

  1994-12-12

• Address:

  No. 191, Jinyang West Road, Lujia Town, Kunshan City, Jiangsu Province

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  91320583608280290E

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  126.271311 yuan

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