Approved on.
Revision Date.
Omeprazole Enteric Dissolve Capsules Instructions
Please read the instructions carefully and use under the guidance of your physician
[Drug Name].
Generic Name: Omeprazole Enteric Capsules
English Name: Omeprazole Enteric Capsules
Hanyu Pinyin: AomeilazuoChangrongJiaonang
[Ingredients
The main ingredient of this product is: Omeprazole.
Chemically: 5-methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridyl)methyl “font-family:Arial”>] thionyl]-1H-benzimidazole
Chemical structure formula.
Molecular Formula: C17H19N3O3S
Molecular weight: 345.42
[Properties] This product is a capsule, the contents of which are white or off-white enteric pills or granules.
[Indications]For gastric ulcer, duodenal ulcer, gastroesophageal reflux disease and Dro-El syndrome (gastrinoma).
[Specification] 20mg
[Dosage].
To be taken orally, not to be chewed.
1. Gastric ulcer, duodenal ulcer: 20mg once, 1 to 2 times a day. Swallow once a day in the morning or once in the morning and once in the evening. The course of treatment is usually 4 to 8 weeks for gastric ulcer and 2 to 4 weeks for duodenal ulcer. In patients with milder symptoms, 10 mg may be used or as directed by the physician.
2. Gastroesophageal reflux disease: 20mg once, 1 to 2 times a day. Swallow once a day in the morning or once in the morning and once in the evening. The course of treatment should be as prescribed by the doctor. After symptoms are controlled, 10mg is available or as prescribed by the doctor.
3.
Liver function impairment
Patients with severe hepatic impairment should take 10mg to 20mg daily.
Renal impairment
Patients with renal impairment do not require dose adjustment.
[Adverse reactions
The most common adverse reactions (occurring in 1-10% of patients) were headache, abdominal pain, constipation, diarrhea, gastrointestinal distention, and nausea/vomiting. Gastric mucosal cell hyperplasia and atrophic gastritis can occur in some long-term treatment cases.
Adverse reactions that have been identified or suspected during clinical trials and post-marketing use of omeprazole are listed below. No dose-related reactions were identified. The adverse reactions listed below are classified according to frequency of occurrence and human organ system (SOC). The frequency categories are defined as follows: very common (≥ 1/10), common (≥ 1/100, < 1/10), occasional (≥ 1/1,000, < 1/100), rare (≥ 1/10,000, < 1/1,000), very rare (< 1/10,000), and Unknown frequency (cannot be estimated from available data).
System organ class/frequencyAdverse reactionsDiseases of the blood and lymphatic systemrareLeukopenia, thrombocytopeniaVery rareGranulocyte Deficiency, PancytopeniaImmune System Disordersrare hypersensitivity reactions (e.g., fever), angioedema, and tachyphylaxis/shockMetabolic and nutritional disordersrareHyponatremiaunknown frequencyhypomagnesemia, severe hypomagnesemia may lead to hypocalcemia, and hypomagnesemia may also be associated with hypokalemiaPsychiatric categoryoccasionalInsomniarare Irritability, confusion, depressionVery rareAttacks, hallucinationsAll types of neurological disordersCommonHeadacheoccasionalDizziness, abnormal sensation, drowsinessrareAbnormal tasteOcular organ diseaserareBlurred visionEar and Labyrinthine Disordersoccasional VertigoRespiratory, thoracic and mediastinal disorders =”padding-left: 7px; padding-right: 7px; border-top: none; border-left: solid 0.5pt; border-bottom: solid 0.5pt; border-right: solid 0.5pt”>rareBronchospasmGastrointestinal DisordersCommonAbdominal pain, constipation, diarrhea, gastrointestinal distention, nausea/vomiting
Gastric fundic gland polyp (benign)rareDry mouth, oral mucositis, gastrointestinal candidiasisunknown frequencyMicroscopic colitisDiseases of the hepatobiliary systemEventuallyElevated liver enzymesrareHepatitis with or without jaundiceVery rareEncephalopathy in patients with liver failure, previous history of liver disease Dermal and subcutaneous tissue disorders occasionalDermatitis, pruritus, rash, urticariarare Hair loss, photosensitivityVery rareErythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis relaxans (TEN) unknown frequencySubacute cutaneous lupus erythematosusVarious musculoskeletal and connective tissue disordersoccasionalHip, wrist, or spine fracturerare Arthralgia, myalgiaVery rareMyasthenia gravisKidney and urinary tract disordersrareInterstitial nephritisReproductive and breast disordersVery rareMale breast developmentSystemic disease and various reactions at the site of administrationoccasionaldiscomfort, peripheral edemarareIncreased sweating[Taboo].
1. Known hypersensitivity to omeprazole, other benzimidazoles, or any other component of this product is contraindicated. Hypersensitivity reactions may include tachyphylaxis, anaphylaxis, angioedema, bronchospasm, interstitial nephritis, and urticaria.
2. As with other proton pump inhibitors, omeprazole should not be combined with nelfinavir and rilpivirine.
[Precautions].
1. Malignant tumors of the stomach
When a gastric ulcer is suspected or confirmed and alarm symptoms (such as significant weight loss, recurrent vomiting, dysphagia, vomiting of blood or black stool) are present, malignancy should be ruled out first.
Adult patients who present with poor remission or early symptom recurrence after completion of PPI therapy should be considered for additional follow-up and diagnostic testing. In older patients, endoscopy needs to be considered.
The presence of gastric malignancy cannot be ruled out in adult patients who have achieved symptomatic remission with this product.
2. Acute interstitial nephritis
Acute interstitial nephritis has been observed in patients taking PPIs (including this product). Acute interstitial nephritis may occur at any time point during PPI therapy and is usually attributed to idiopathic hypersensitivity reactions. If acute interstitial nephritis occurs, discontinue treatment with this product.
3. Clostridium difficile-associated diarrhea
Published observational studies suggest that PPI therapy (such as this product) may increase the risk of Clostridium difficile-associated diarrhea (CDAD), especially in hospitalized patients. If diarrhea does not improve, the diagnosis should be considered.
4. Cyanocobalamin (vitamin B-12) deficiency
Long-term (e.g., more than 3 years) daily treatment with an antacid may result in cyanocobalamin (vitamin B-12) malabsorption due to decreased or deficient gastric acid. Rare reports of cyanocobalamin deficiency with acid suppression therapy have been reported in the reference literature. This diagnosis should be considered if clinical signs consistent with cyanocobalamin deficiency are observed in patients treated with this product.
5. Combination of clopidogrel
The combination of this product and clopidogrel should be avoided. Clopidogrel is a precursor drug. The platelet agglutination inhibition produced by clopidogrel can be attributed solely to its active metabolite. The combined use of drugs that inhibit CYP2C19 activity (e.g., omeprazole) can impair the metabolism of clopidogrel into its active metabolite. Coadministration of clopidogrel and 80 mg omeprazole decreases the pharmacologic activity of clopidogrel, even when the two are administered 12 hours apart. Therefore, other antiplatelet therapy should be considered when using this product.
6. Combination of St. John’s wort or rifampin
Drugs that induce CYP2C19 or CYP3A4 (e.g., St. John’s wort or rifampin) can significantly reduce omeprazole blood levels (see [Drug Interactions]). This product should be avoided in combination with St. John’s wort or rifampin.
7. Combination of methotrexate
The literature suggests that the combination of PPIs and methotrexate (mainly at high doses) may increase serum concentrations of methotrexate and/or its metabolites, prolong the duration of high serum concentrations, and may lead to methotrexate toxicity. Temporary discontinuation of PPIs may be considered in some patients on high doses of methotrexate.
8. Co-administration of atazanavir
Co-administration of proton pump inhibitors with atazanavir is not recommended. If combination use is unavoidable, close clinical monitoring (e.g., viral load) is recommended, along with increasing the dose of atazanavir to 400 mg, adding 100 mg of ritonavir, and the omeprazole dose should not exceed 20 mg.
9. Hypomagnesemia
Rare cases of asymptomatic and symptomatic hypomagnesemia have been reported in patients treated with PPIs for at least 3 months (the vast majority after 1 year of treatment). Serious adverse events included hand and foot twitching, cardiac arrhythmias, and seizures. For most patients, correction of hypomagnesemia requires magnesium supplementation and discontinuation of PPIs.
Regular monitoring of blood magnesium concentrations needs to be considered in anticipation of prolonged PPI therapy or with comorbid medications such as digoxin or drugs that may cause hypomagnesemia (e.g., diuretics).
10. Fractures
Several published observational studies suggest that treatment with proton pump inhibitors (PPIs) may put people at increased risk of fractures in areas such as the hip, wrist, or spine due to osteoporosis. For patients treated with high doses (defined as multiple daily doses) and long-term PPI therapy (1 year or more), there is an increased risk of fracture. Patients should be treated with the lowest dose and shortest course of PPI therapy appropriate for the treatment situation. Patients who are at risk for osteoporosis-related fractures should be treated according to existing guidelines.
11. Skin and systemic lupus erythematosus
Cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE) have been reported in patients taking PPIs, including this product, with CLE being more common than SLE. Such events are both new onset and worsening of existing autoimmune disease. The most common type of CLE is subacute CLE (SCLE), which often occurs within weeks to years after continuous drug therapy and develops in a population ranging from infants to elderly patients. In general, histologic findings are observed without organ involvement.
The severity of PPI-associated SLE is usually less severe than that of non-drug-induced SLE. Most patients present with only a rash, but arthralgia and hemocytopenia have been reported.
PPI analogs should be avoided for longer than clinically necessary, and if signs or symptoms consistent with CLE or SLE are observed in patients receiving this product, the drug should be discontinued and the patient should be referred to the appropriate specialist for evaluation. for evaluation. within 4 to 12 weeks of PPI monotherapy discontinuation, most patients’ symptoms will improve. It may take longer for elevated serologic findings to resolve compared to the clinical presentation.
12. Interaction with diagnostic tests for neuroendocrine tumors
Serum chromogranin A (CgA) levels are elevated secondary to drug-induced lowering of gastric acid. elevated CgA levels can lead to false-positive diagnostic tests for neuroendocrine tumors. Healthcare professionals should suspend omeprazole use for at least 14 days prior to evaluating blood CgA levels and consider retesting this indicator if the initial test CgA level is elevated. Because normal reference values may vary between laboratories, if a series of tests (e.g., monitoring) is needed, they should be performed in the same laboratory.
13. This product contains lactose. Patients with rare genetic disorders such as galactose intolerance, Lapp lactase deficiency, or glucose-galactose malabsorption should not take this product.
14. Patients who have been taking this product for a long time, especially if they have been using it for more than 1 year, should be monitored regularly.
15. Treatment with proton pump inhibitors may result in a slightly increased risk of gastrointestinal infections such as Salmonella and Campylobacter.
16. This product is an enteric coated capsule; be careful not to chew it when taking it to avoid premature release of the drug in the stomach and compromise its efficacy.
17. Effects on driving and mechanical ability: This product basically does not affect the ability to drive or operate machinery. Adverse drug reactions such as dizziness and visual disturbances may occur. If affected, patients should not drive or operate machinery.
[For pregnant and lactating women
Pregnant women: There are no adequate and well-controlled controlled studies of this product in pregnant women. The available epidemiologic data fail to demonstrate that omeprazole use early in pregnancy increases the risk of significant congenital teratogenicity or leads to other adverse pregnancy outcomes. Because of the effects of high-dose esomeprazole magnesium on the developing skeleton observed in rat studies, it should be used during pregnancy only if the potential benefit to the fetus outweighs the potential risk.
Lactation: Omeprazole may be secreted into breast milk, but there are no clinical data on the effect of omeprazole on breastfed infants or on lactation. The clinical need of the mother for this product and the potential adverse effects of this product or maternal underlying disease on the breastfed infant should be weighed along with the developmental and health benefits of breastfeeding and should be used only if the benefits outweigh the potential risks.
[Pediatric Use
This trial has not been conducted in China and there are no reliable references.
[Geriatric use].
No dose adjustment is required in elderly patients.
[Drug Interactions
1. Effect of omeprazole on the pharmacokinetics of other active substances
(1) pH-dependent absorption of the active substance.
During omeprazole treatment, a decrease in gastric acid may facilitate or inhibit the absorption of active substances that present gastric pH-dependent absorption.
Nelfinavir, atazanavir.
The blood levels of nelfinavir and atazanavir are reduced when used in combination with omeprazole.
The combination of omeprazole and nelfinavir is contraindicated. Co-administration of omeprazole (40 mg once daily) reduced mean exposure to nelfinavir by approximately 40% and mean exposure to the pharmacologically active metabolite M8 by approximately 75%-90%. Interactions may also include inhibition of CYP2C19.
Co-administration of omeprazole and atazanavir is not recommended. In healthy volunteers, the combination of omeprazole (40 mg once daily) and atazanavir 300 mg/ritonavir 100 mg resulted in a 75% reduction in atazanavir exposure. An increase in the atazanavir dose to 400 mg did not compensate for the effect of omeprazole on atazanavir exposure. In healthy volunteers, the combination of omeprazole (20 mg once daily) and atazanavir 400 mg/ritonavir 100 mg reduced atazanavir exposure by approximately 30% compared with atazanavir 300 mg/ritonavir 100 mg (once daily).
Digoxin.
Concurrent administration of omeprazole (20 mg once daily) with digoxin in healthy subjects resulted in a 10% increase in digoxin bioavailability. Digoxin toxicity has rarely been reported. However, caution should be exercised when high doses of omeprazole are given to elderly patients. If a combination is necessary, therapeutic drug monitoring of digoxin should be intensified.
Clopidogrel.
Results from studies in healthy subjects showed a pharmacokinetic (PK)/pharmacodynamic (PD) interaction between clopidogrel (300 mg loading dose/75 mg daily maintenance dose) and omeprazole (80 mg daily orally) ( PD) interaction resulted in an average 46% decrease in exposure to the active metabolite of clopidogrel and led to an average 16% decrease in maximal inhibition of platelet aggregation (ADP induction).
Discrepant data have been reported from both observational and clinical studies regarding the clinical significance of omeprazole and clopidogrel PK/PD interactions in major cardiovascular events. Concomitant use of omeprazole and clopidogrel should be avoided.
Other drugs.
In combination with omeprazole, the absorption of posaconazole, erlotinib, ketoconazole, and itraconazole is significantly reduced, which may affect their clinical efficacy. The combination of posaconazole and erlotinib with this product should be avoided.
(2) Active substances metabolized by CYP2C19.
Omeprazole is a moderately potent inhibitor of CYP2C19, the primary metabolizing enzyme of omeprazole. Therefore, the combination of active substances that are also metabolized by CYP2C19 decreases their metabolism, which in turn increases the systemic exposure to these substances. Such drugs include R-warfarin and other vitamin K antagonists, cilostazol, diazepam, and phenytoin.
Cilostazol.
In a crossover study, healthy subjects receiving a 40 mg dose of omeprazole increased the Cmax and AUC of cilostazol by 18% and 26%, respectively, and one of the active metabolite increased by 29% and 69%, respectively.
Phenytoin.
Phenytoin blood levels are recommended to be monitored during the first two weeks after initiation of omeprazole therapy, and if phenytoin dose adjustment is performed, it should be monitored and further adjusted after the end of omeprazole therapy.
(3) Unknown mechanism
Saquinavir.
Omeprazole in combination with saquinavir/ritonavir resulted in an approximately 70% increase in saquinavir blood levels, associated with good tolerability in HIV-infected patients.
Tacrolimus.
Co-administration of omeprazole can increase tacrolimus blood levels. Monitoring of tacrolimus concentrations and renal function (creatinine clearance) should be intensified, and tacrolimus doses should be adjusted if necessary.
Methotrexate.
Increased methotrexate levels have been reported in some patients when combined with proton pump inhibitors. Temporary discontinuation of omeprazole may be considered when high doses of methotrexate are given.
2. Effect of other active substances on omeprazole pharmacokinetics
(1) CYP2C19 and/or CYP3A4 inhibitors.
Because omeprazole is metabolized via CYP2C19 and CYP3A4, active drugs known to inhibit CYP2C19 or CYP3A4 (e.g., clarithromycin and voriconazole) may reduce the rate of metabolism of omeprazole This in turn leads to increased omeprazole blood levels. The combination of voriconazole may at least double the exposure to omeprazole. Because high doses of omeprazole are well tolerated, there is generally no need to adjust the omeprazole dose. However, in patients with severe hepatic impairment, dose adjustment should be considered if long-term therapy is required.
(2) CYP2C19 and/or CYP3A4 inducers:
Active drugs known to induce CYP2C19 and/or CYP3A4 (e.g., rifampin and St. John’s wort) can increase the rate of omeprazole metabolism, which in turn leads to a decrease in omeprazole blood levels.
[Drug overdose
Information on the effects of omeprazole drug overdose in humans is limited. Doses as high as 560 mg have been reported in the literature, with occasional reports of single oral doses up to 2400 mg (a dose that is 120 times the recommended clinical routine). Clinical manifestations of omeprazole overdose are highly variable and include nausea, vomiting, dizziness, abdominal pain, diarrhea, headache, apathy, depression, confusion, drowsiness, blurred vision, tachycardia, sweating, flushing, and dry mouth.
The symptoms described were all transient, and no cases of serious clinical outcome were reported. Clearance (primary pharmacokinetics) remained unchanged with increasing dose. There is no known specific antidote for omeprazole overdose. Because omeprazole is extensively bound to plasma proteins in vivo, an overdose of omeprazole is not readily cleared by dialysis. If an overdose occurs, symptomatic treatment and supportive therapy should be given.
[Pharmacology and Toxicology].
Pharmacological effects
Omeprazole is a benzimidazole-like compound that blocks gastric acid secretion by specifically inhibiting the H+-K+ ATPase system in gastric lining cells. final step. The effect is dose-dependent and inhibits both basal and stimulated gastric acid secretion.
Microbiology
Omeprazole in diphasic combination with clarithromycin or triple combination of omeprazole, clarithromycin and amoxicillin is effective against most H. pylori strains in in vitro trials as well as clinically.
Toxicological studies
Genotoxicity.
Omeprazole Ames assay, mouse lymphoma cell assay and rat liver DNA damage assay showed negative results, and in vitro human lymphocyte chromosome aberration assay, 1 of 2 mouse micronucleus assays and in vivo mouse bone marrow cell chromosome The test results were positive.
Reproductive toxicity.
Rats given orally 138 mg/kg/day of omeprazole (approximately 34 times the human oral dose of 40 mg based on body surface area) showed no significant abnormalities in fertility or reproductive behavior.
Omeprazole 138 mg/kg/day (approximately 34 times the human oral dose of 40 mg on a body surface area basis) was given orally to pregnant rats and 69 mg/kg/day (approximately 34 times the human oral dose of 40 mg on a body surface area basis) to pregnant rabbits. The potential teratogenic effect of omeprazole was not found in pregnant rabbits given 69 mg/kg/day (approximately 34 times the human oral dose of 40 mg on a surface area basis).
Rabbits given omeprazole 6.9-69.1 mg/kg/day (approximately 3.4-34 times the human oral dose of 40 mg on a body surface area basis) showed a dose-dependent increase in embryonic mortality, fetal resorption, and abortion rates.
Dose-dependent embryo/fetus toxicity was seen in offspring of parental rats given omeprazole 13.8-138.0 mg/kg/day (approximately 3.4-34 times the human oral dose of 40 mg on a body surface area basis) and postnatal developmental toxicity.
Carcinogenicity.
Omeprazole doses of 1.7, 3.4, 13.8, 44.0, and 140.8 mg/kg/day (approximately 0.4- to 40 mg of the human oral dose, based on body surface area) in two 2-year carcinogenicity tests in rats were 34 times the human oral dose of 40 mg), gastrointestinal chromophobe (ECL) cell carcinoids appeared dose-dependently in both males and females; the incidence was significantly higher in females than in males, and the blood concentrations of omeprazole were higher in females than in males. Gastric carcinoid tumors were rarely seen in unadministered animals, whereas ECL cell hyperplasia was seen in both female and male administered groups.
In another trial, female rats were given omeprazole 13.8 mg/kg/day (approximately 3.4 times the human oral dose of 40 mg on a body surface area basis) for 1 year, followed by 1 year of discontinuation, and no carcinoid tumors were seen. However, drug-related ECL cell hyperplasia occurred in rats at 1 year of administration (94% in the dosed group and 10% in the control group), and the difference between the dosed and control groups narrowed by the second year, although the incidence of ECL cell hyperplasia was still higher in the dosed group (46%/26%). gastric adenocarcinoma developed in one rat (2%) and was not seen in either male or female rats at 2 years of dosing. Historically, no similar tumors have been documented in rats of this species, and since only one case occurred, its significance is difficult to judge. In a 52-week toxicity test in SD rats, omeprazole doses of 0.4, 2, and 16 mg/kg/day (approximately 0.1-3.9 times the human oral dose of 40 mg based on body surface area) resulted in a small number of brain astrocytomas in males, but not in females. In a 2-year carcinogenicity test in SD rats at a maximum dose of 140.8 mg/kg/day (approximately 34 times the human oral dose of 40 mg on a body surface area basis), astrocytomas were not seen in males or females.
No increase in tumor incidence was seen in the 78-week carcinogenicity test in omeprazole mice, but the results of this test were inconclusive. p53 (+/-) transgenic mice had negative results in the 26-week carcinogenicity test.
Young animal test.
Young rats were given esomeprazole magnesium at a dose of 70-280 mg/kg/day (approximately 17-68 times the human oral dose of 40 mg based on body surface area) for 28 consecutive days from postnatal day 7 to day 35 days, with a recovery period of 14 days. The results showed an increase in the number of dead animals in the highest dose group. In addition, at 140 mg/kg/day (approximately 34 times the human oral dose of 40 mg based on body surface area) and higher doses, a decrease in body weight and weight gain, a decrease in femur weight and length, and an impact on overall growth were seen.
Similar results were seen with estramiprazole strontium at equimolar doses in the above tests.
[Pharmacokinetics
1. Absorption
Omeprazole and omeprazole magnesium are not acid-resistant and are therefore administered orally as enteric-coated pellets in capsules or tablets. Omeprazole is rapidly absorbed, with peak blood concentrations observed approximately 1-2 hours after administration. Omeprazole is absorbed in the small intestine and is usually completely absorbed within 3-6 hours. Simultaneous ingestion of food has no effect on its bioavailability. The systemic availability (bioavailability) of a single oral dose of omeprazole is approximately 40%. After repeated once-daily dosing, bioavailability increased to approximately 60%.
2. Distribution
The apparent volume of distribution in healthy subjects was approximately 0.3 l/kg body weight. Omeprazole plasma protein binding was 97%.
3. Biotransformation
Omeprazole is completely metabolized by the cytochrome P450 system (CYP). The major part of its metabolism depends on the polymorphic expression of CYP2C19, which is responsible for the formation of the major metabolite hydroxy omeprazole in plasma. The remaining part depends on another specific isoform, CYP3A4, which is responsible for the production of omeprazole sulfone. Due to the high affinity of omeprazole to CYP2C19, there is a potential for competitive inhibition and drug interactions with other substrates of CYP2C19. However, due to the low affinity for CYP3A4, omeprazole does not potentially inhibit the metabolism of other CYP3A4 substrates. In addition, omeprazole does not inhibit the major CYP enzymes.
About 3% of the Caucasian population and 15-20% of the Asian population lack functional CYP2C19 enzymes and are referred to as slow metabolizers. In such individuals, the metabolism of omeprazole is likely to be catalyzed primarily through CYP3A4. After repeated administration of omeprazole at a dose of 20 mg once daily, the mean AUC was approximately 5-10 times higher in slow metabolizers than in subjects with a functional CYP2C19 enzyme (fast metabolizers), and the mean blood peak concentration was also as high as 3 to 5 times higher. These results have no impact on omeprazole dose selection.
4. Excretion
The plasma elimination half-life of omeprazole is usually shorter than 1 hour after single and once-daily repeated dosing. Omeprazole was completely eliminated from plasma at various doses, with no tendency to accumulate during once-daily dosing. Almost 80% of the oral dose of omeprazole is excreted in the urine as metabolites, with the remainder excreted from the feces after secretion by bile.
5. Linear/nonlinear
The AUC of omeprazole increases with repeated dosing. This increase was dose-dependent, with a non-linear dose-AUC relationship after repeated dosing. The above time and dose dependence is most likely due to a decrease in first pass elimination and systemic clearance due to the inhibition of CYP2C19 enzyme by omeprazole and/or its metabolites (e.g., sulfone). No effect of metabolites on gastric acid secretion was observed.
[Storage] Shade, seal, and store in a dry place.
[Packaging] Oral solid medicine in HDPE bottle (with desiccant), 7 capsules/bottle/box, 14 capsules/bottle/box.
[Expiration date] 24 months
[Executive Standard
[Approval number] 国家药准字H10920092
[Manufacturer
Company Name: Haihailing Chemical Pharmaceutical Co.
Manufacturing Address: No.281, Nanhai Avenue, Haikou City, Hainan Province
Postal Code:570311
Tel:0898-68639900
Fax Number:0898-66792859
Website:www.hailingpharm.com