英文药名：BUPHENYL（SODIUM PHENYLBUTYRATE）

中文药名：苯丁酸钠片/粉  苯基丁酸钠

生产厂家：MEDICIS

给药说明
1996年FDA批准在美国上市的新药，商品名Buphenyl powder (Ucyclyd Pharma）。该品对于因氨基甲酰磷酸合成酶(CPS）、鸟氨酸氨甲酰转移酶（OTC）或精氨基琥珀酸合成酶（AS）缺乏而致慢性脲循环紊乱的病人，可用作辅助治疗.
本药为乙酸苯酯的前体药物，主要用于尿素循环障碍的附加治疗。通过调整饮食中氮摄入量及使用本类药物以排泄体内的废氮产物，可以减少尿素循环障碍患者的尿素合成。其具体作用机制如下：本药在体内经β-氧化代谢成乙酸苯酯，乙酸苯酯继而与谷氨酰氨共轭生成苯乙酰谷氨酰氨，上述2步反应均较快而完全。苯乙酰谷氨酰氨作为尿素的替代废氮产物，可通过肾脏排泄，与尿素在摩尔水平上相比，两者每摩尔均含有2摩尔氮(即1摩尔本药也可以清除2摩尔氨基酸来源的氮)。据报道，使用本药治疗尿素循环障碍患者(联合控制饮食氮摄入量)，血氨及血谷氨酸水平可有降低甚至达正常水平。

苯基丁酸钠粉与片 欧洲商标名 Ammonaps (sodium phenylbutyrate)，美国商标名 Buphenyl
Sodium Phenylbutyrate Tablet          
英文商品名：Buphenyl®
中文商品名：無
主成分：sodium phenylbutyrate。
劑型：
錠劑，500 mg；粉末，每茶匙含3 gmsodium phenylbutyrate。
適應症：
缺乏carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC)或argininosuccinic acid synthetase主要是做為尿素循環障礙(urea cycle disorder)病人的輔助性治療。
藥理機轉：本品為無味的化合物，在體內會經由β氧化作用而代謝成phenylacetate；之後phenylacetate再和glutamine結合形成phenylacetylglutamine。Phenylacetylglutamine代替尿素，將氮經由腎臟排出體外。每個sodium phenylbutyrate分子可以排除兩個amino nitrogen group。有報告指出，尿素循環障礙病人以本品治療(同時限制飲食中氮的攝取)，血中ammonium及glutamine濃度顯著減少或正常化。這類病人的治療方式主要是藉由修正飲食中氮的攝取來減少尿素的合成，及藉由像本品的因子來作為氮排泄的替代路徑。雖然本品效果很好，但在臨床上的用途受限於其會有令人討厭的體臭，而使得病人使用的意願不高。
藥動學：
藥物血中濃度：
達到血中最高濃度的時間：錠劑：口服後1.35小時；粉末：1小時。
ADME：
（1）分佈：分佈體積0.2 L/kg。
（2）代謝：主要在腎臟和肝臟。本品經過β氧化作用，代謝成phenylacetate，之後phenylacetate再和glutamine結合形成phenylacetylglutamine。這個代謝物代替尿素，將氮經由腎臟排出體外。
（3）排除：腎臟，大部分吸收進體內的藥物會在24小時內，以phenylacetylglutamine形式排出體外﹔只有極少部分(<1%)是以phenylbutyrate，或phenylacetate形式排除。乳汁：授乳的安全性未知。
半衰期：phenylbutyrate 0.8小時；phenylacetate 1.2小時。
禁忌：不可用於急性高血氨症之緊急治療。對本品或其代謝物過敏者。嚴重高血壓、心臟衰竭、或腎功能不全者。
副作用：
血液方面：再生性不良貧血。
心血管方面：足踝或週邊水腫、心律不整、昏厥。
中樞神經：頭痛、憂鬱、疲倦、頭昏眼花、失去方向感、記憶力受損。
代謝/內分泌：低白蛋白血症、代謝性酸中毒、代謝性鹼中毒、高氯血症、體重增加。
腸胃方面：食慾減退、腹部疼痛、噁心、嘔吐、胃炎。
腎臟/泌尿道：經期不規則、無月經、腎小管酸血症。
肝臟方面：肝毒性。
皮膚方面：皮疹。
其他：體臭。
懷孕分級：C
交互作用：資料尚未建立。
注意事項：
本品每錠含鈉62 mg。每100 gm粉末含鈉11.7 gm。
病人有輕到中度高血壓、腎功能不全、心衰竭、或其他與鈉滯留有關的水腫現象，應謹慎使用。
肝臟功能不全者，應謹慎使用。
正在服用haloperidol、valproate、或corticosteroid的病人(服用這些藥物可能會造成高血氨症)應謹慎使用。
正在服用probenecid的病人(會影響本品及其代謝物的排除)，應謹慎使用。
肥胖者應謹慎使用。
治療期間血中glutamine濃度應維持低於1000 micromol/L。
用法用量：
1. 正常劑量：20公斤以下的尿素循環障礙病人，建議口服劑量為每天450 ~ 600 mg/kg；20公斤以上的病人則是每天9.9 ~ 13 gm/m2。分次與飲食一起給予。粉末配方可以與食物混合(固體或液體)，但應避免使用酸性飲料。錠劑是設計用於成人及體重大於20 kg兒童處方。粉末配方則是用於口服和經胃造口術或鼻胃管服用的處方。每日劑量超過20 gm的有效性或安全性尚未評估。除非病人接受肝臟移植，否則應該考慮終生治療。
2. 肝功能不者劑量：使用在沒有尿素循環障礙病人中，本品的代謝及排泄不會因肝功能障礙而改變，一般認為不需要調整劑量。然而，還需要更多的藥物動力學方面的評估。
保存：儲存於15℃~ 30℃；開封後，應保持藥瓶緊閉。
廠商：
Buphenyl®
製造廠：UCYCLYD PHARMA, INC.
地址：SCOTTSDALE, AZ 85258

Buphenyl
Generic Name: sodium phenylbutyrate
Dosage Form: powder, tablets
Buphenyl® (sodium phenylbutyrate) Tablets
Buphenyl® (sodium phenylbutyrate) Powder
[ bu'fen-əl ]
(sodium phenylbutyrate)
Rx Only
Buphenyl Description
Buphenyl® (sodium phenylbutyrate) Tablets for oral administration and Buphenyl® (sodium phenylbutyrate) Powder for oral, nasogastric, or gastrostomy tube administration contain sodium phenylbutyrate. Sodium phenylbutyrate is an off-white crystalline substance which is soluble in water and has a strong salty taste. Sodium phenylbutyrate also is freely soluble in methanol and practically insoluble in acetone and diethyl ether. It is known chemically as 4-phenylbutyric acid, sodium salt with a molecular weight of 186 and the molecular formula C10H11O2Na.
Chemical Structure:
Each tablet of Buphenyl contains 500 mg of sodium phenylbutyrate and the inactive ingredients microcrystalline cellulose NF, magnesium stearate NF, and colloidal silicon dioxide NF.
Each gram of Buphenyl Powder contains 0.94 grams of sodium phenylbutyrate and the inactive ingredients calcium stearate NF, and colloidal silicon dioxide NF.
Buphenyl - Clinical Pharmacology
Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to phenylacetate. Phenylacetate is a metabolically-active compound that conjugates with glutamine via acetylation to form phenylacetylglutamine. Phenylacetylglutamine then is excreted by the kidneys. On a molar basis, it is comparable to urea (each containing two moles of nitrogen). Therefore, phenylacetylglutamine provides an alternate vehicle for waste nitrogen excretion.
PHARMACOKINETICS
General
Pharmacokinetic studies have not been conducted in the primary patient population (neonates, infants, and children), but pharmacokinetic data were obtained from normal adult subjects.
Absorption
Peak plasma levels of phenylbutyrate occur within 1 hour after a single dose of 5 grams of sodium phenylbutyrate tablet with a Cmax of 218 µg/mL under fasting conditions; peak plasma levels of phenylbutyrate occur within 1 hour after a single dose of 5 grams of sodium phenylbutyrate powder with a Cmax of 195 µg/mL under fasting conditions. The effect of food on phenylbutyrate's absorption is unknown.
Disposition
The overall disposition of sodium phenylbutyrate and its metabolites has not been characterized fully. However, the drug is known to be metabolized to phenylacetate and subsequently to phenylacetylglutamine. Following oral administration of 5 grams (tablets), measurable plasma levels of phenylbutyrate and phenylacetate were detected 15 and 30 minutes after dosing, respectively, and phenylacetylglutamine was detected shortly thereafter. The pharmacokinetic parameters for phenylbutyrate for Cmax (µg/mL), Tmax (hours), and elimination half-life (hours) were 218, 1.35, and 0.77, respectively, and for phenylacetate were 48.5, 3.74, and 1.15, respectively.
Following oral administration of 5 grams of the powder, measurable plasma levels of phenylbutyrate and phenylacetate were detected 15 and 30 minutes after dosing, respectively, and phenylacetylglutamine was detected shortly thereafter. The pharmacokinetic parameters for phenylbutyrate for Cmax (µg/mL), Tmax (hours), and elimination half-life (hours) were 195, 1.00, and 0.76, respectively, and for phenylacetate were 45.3, 3.55, and 1.29, respectively.
The major sites for metabolism of sodium phenylbutyrate are the liver and kidney.
Excretion
A majority of the administered compound (approximately 80 – 100%) was excreted by the kidneys within 24 hours as the conjugation product, phenylacetylglutamine. For each gram of sodium phenylbutyrate administered, it is estimated that between 0.12 – 0.15 grams of phenylacetylglutamine nitrogen are produced.
Pharmacodynamics
In patients with urea cycle disorders, Buphenyl® decreased elevated plasma ammonia glutamine levels. It increases waste nitrogen excretion in the form of phenylacetylglutamine.
Special Populations
Gender
Significant gender differences were found in the pharmacokinetics of phenylbutyrate and phenylacetate, but not for phenylacetylglutamine. The pharmacokinetic parameters (AUC and Cmax), for both plasma phenylbutyrate and phenylacetate were about 30 to 50 percent greater in females than in males.
Hepatic insufficiency
In patients who did not have urea cycle disorders but had impaired hepatic function, the metabolism and excretion of sodium phenylbutyrate were not affected. However, this information was obtained from unvalidated, uncontrolled case studies.
Indications and Usage for Buphenyl
Buphenyl® is indicated as adjunctive therapy in the chronic management of patients with urea cycle disorders involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS). It is indicated in all patients with neonatal-onset deficiency (complete enzymatic deficiency, presenting within the first 28 days of life). It is also indicated in patients with late-onset disease (partial enzymatic deficiency, presenting after the first month of life) who have a history of hyperammonemic encephalopathy. It is important that the diagnosis be made early and treatment initiated immediately to improve survival. Any episode of acute hyperammonemia should be treated as a life-threatening emergency.
Buphenyl must be combined with dietary protein restriction and, in some cases, essential amino acid supplementation. (See Nutritional Supplementation subsection of the DOSAGE AND ADMINISTRATION section.)
Previously, neonatal-onset disease was almost universally fatal within the first year of life, even when treated with peritoneal dialysis and essential amino acids or their nitrogen-free analogs. However, with hemodialysis, use of alternative waste nitrogen excretion pathways (sodium phenylbutyrate, sodium benzoate, and sodium phenylacetate), dietary protein restriction, and, in some cases, essential amino acid supplementation, the survival rate in newborns diagnosed after birth but within the first month of life is almost 80%. Most deaths have occurred during an episode of acute hyperammonemic encephalopathy. Patients with neonatal-onset disease have a high incidence of mental retardation. Those who had IQ tests administered had an incidence of mental retardation as follows: ornithine transcarbamylase deficiency, 100% (14/14 patients tested); argininosuccinic acid synthetase deficiency, 88% (15/17 patients tested); and carbamylphosphate synthetase deficiency, 57% (4/7 patients tested). Retardation was severe in the majority of the retarded patients.
In patients diagnosed during gestation and treated prior to any episode of hyperammonemic encephalopathy, survival is 100%, but even in these patients, most subsequently demonstrate cognitive impairment or other neurologic deficits.
In late-onset deficiency patients, including females heterozygous for ornithine transcarbamylase deficiency, who recover from hyperammonemic encephalopathy and are then treated chronically with sodium phenylbutyrate and dietary protein restriction, the survival rate is 98%. The two deaths in this group of patients occurred during episodes of hyperammonemic encephalopathy. However, compliance with the therapeutic regimen has not been adequately documented to allow evaluation of the potential for Buphenyl and dietary protein restriction to prevent mental deterioration and recurrence of hyperammonemic encephalopathy if carefully adhered to. The majority of these patients tested (30/46 or 65%) have IQ's in the average to low average/borderline mentally retarded range. Reversal of pre-existing neurologic impairment is not likely to occur with treatment and neurologic deterioration may continue in some patients.
Even on therapy, acute hyperammonemic encephalopathy recurred in the majority of patients for whom the drug is indicated.
Buphenyl may be required life-long unless orthotopic liver transplantation is elected.
(See CLINICAL PHARMACOLOGY, Pharmacodynamics subsection for the biochemical effects of Buphenyl).
Contraindications
Buphenyl® should not be used to manage acute hyperammonemia, which is a medical emergency.
Warnings
Each Buphenyl® Tablet contains 62 mg of sodium (9.2% w/w) (corresponding to 124 mg of sodium per gram of sodium phenylbutyrate [12.4% w/w]) and Buphenyl Powder contains 11.7 grams of sodium per 100 grams of powder, corresponding to 125 mg of sodium per gram of sodium phenylbutyrate (12.4% w/w). Buphenyl should be used with great care, if at all, in patients with congestive heart failure or severe renal insufficiency, and in clinical states in which there is sodium retention with edema.
Because Buphenyl is metabolized in the liver and kidney,andphenylacetylglutamine is primarily excreted by the kidney, use caution when administering the drug to patients with hepatic or renal insufficiency or inborn errors of beta oxidation. Probenecid is known to inhibit the renal transport of many organic compounds, including hippuric acid, and may affect renal excretion of the conjugated product of Buphenyl as well as its metabolite.
Use of corticosteroids may cause the breakdown of body protein and increase plasma ammonia levels.
Precautions
General
Buphenyl® should not be administered to patients with known hypersensitivity to sodium phenylbutyrate or any component of this preparation.
There have been published reports of hyperammonemia being induced by haloperidol and by valproic acid.
Neurotoxicity of phenylacetate in animals
When given subcutaneously to rat pups, 190–474 mg/kg phenylacetate caused decreased proliferation and increased loss of neurons, and it reduced CNS myelin. Cerebral synapse maturation was retarded, and the number of functioning nerve terminals in the cerebrum was reduced, which resulted in impaired brain growth. Prenatal exposure of rat pups to phenylacetate produced lesions in layer 5 of the cortical pyramidal cells; dendritic spines were longer and thinner than normal and reduced in number.
Information for Patients
The full text of the separate insert of information for patients is reprinted at the end of the labeling.
Laboratory Tests
Plasma levels of ammonia, arginine, branched-chain amino acids, and serum proteins should be maintained within normal limits, and plasma glutamine should be maintained at levels less than 1,000 µmol/L. Serum drug levels of phenylbutyrate and its metabolites, phenylacetate and phenylacetylglutamine, should be monitored periodically.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Carcinogenicity, mutagenicity, and fertility studies of sodium phenylbutyrate have not been conducted.
Pregnancy
Pregnancy Category C.
Animal reproduction studies have not been conducted with Buphenyl®. It is also not known whether Buphenyl can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity.
Buphenyl should be given to a pregnant woman only if clearly needed.
Nursing Mothers
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Buphenyl® is administered to a nursing woman.
Pediatric Use
The use of tablets for neonates, infants and children to the weight of 20 kg is not recommended. (See Dosage and Administration.)
Adverse Reactions
The assessment of clinical adverse events came from 206 patients treated with sodium phenylbutyrate. Adverse events (both clinical and laboratory) were not collected systematically in these patients, but were obtained from patient-visit reports by the 65 co-investigators. Causality of adverse effects is sometimes difficult to determine in this patient population because they may result from either the underlying disease, the patient's restricted diet, intercurrent illness, or Buphenyl®. Furthermore, the rates may be under-estimated because they were reported primarily by parent or guardian and not the patient.
Clinical Adverse Events
In female patients, the most common clinical adverse event reported was amenorrhea/menstrual dysfunction (irregular menstrual cycles), which occurred in 23% of the menstruating patients.
Decreased appetite occurred in 4% of all patients. Body odor (probably caused by the metabolite, phenylacetate) and bad taste or taste aversion were each reported in 3% of patients.
Other adverse events reported in 2% or fewer patients were:
Gastrointestinal: abdominal pain, gastritis, nausea and vomiting; constipation, rectal bleeding, peptic ulcer disease, and pancreatitis each occurred in one patient.
Hematologic: aplastic anemia and ecchymoses each occurred in one patient.
Cardiovascular: arrhythmia and edema each occurred in one patient.
Renal: renal tubular acidosis
Psychiatric: depression
Skin: rash
Miscellaneous: headache, syncope, and weight gain
Neurotoxicity was reported in cancer patients receiving intravenous phenylacetate, 250–300 mg/kg/day for 14 days, repeated at 4-week intervals. Manifestations were predominately somnolence, fatigue, and lightheadedness; with less frequent headache, dysgeusia, hypoacusis, disorientation, impaired memory, and exacerbation of a pre-existing neuropathy. These adverse events were mainly mild in severity. The acute onset and reversibility when the phenylacetate infusion was discontinued suggest a drug effect.
Laboratory Adverse Events
In patients with urea cycle disorders, the frequency of laboratory adverse events by body system were:
Metabolic: acidosis (14%), alkalosis and hyperchloremia (each 7%), hypophosphatemia (6%), hyperuricemia and hyperphosphatemia (each 2%), and hypernatremia and hypokalemia (each 1%).
Nutritional: hypoalbuminemia (11%) and decreased total protein (3%).
Hepatic: increased alkaline phosphatase (6%), increased liver transaminases (4%), and hyperbilirubinemia (1%).
Hematologic: anemia (9%), leukopenia and leukocytosis (each 4%), thrombocytopenia (3%), and thrombocytosis (1%).
The clinician is advised to routinely perform urinalysis, blood chemistry profiles, and hematologic tests.
Overdosage
No adverse experiences have been reported involving overdoses of sodium phenylbutyrate in patients with urea cycle disorders.
In the event of an overdose, discontinue the drug and institute supportive measures.
Hemodialysis or peritoneal dialysis may be beneficial.
Buphenyl Dosage and Administration
For oral use only.
The use of Buphenyl® Tablets is indicated for children weighing more than 20 kg and for adults.
The usual total daily dose of Buphenyl Tablets and Powder for patients with urea cycle disorders is 450 – 600 mg/kg/day in patients weighing less than 20 kg, or 9.9 –13.0 g/m2/day in larger patients. The tablets and powder are to be taken in equally divided amounts with each meal or feeding (i.e., three to six times per day).
Buphenyl® Powder is indicated for oral use (via mouth, gastrostomy, or nasogastric tube) only.   The powder is to be mixed with food (solid or liquid) for immediate use; however, when dissolved in water, Buphenyl Powder has been shown to be stable for up to one week at room temperature or refrigerated. Sodium phenylbutyrate is very soluble in water (5 grams per 10 mL). When Buphenyl Powder is added to a liquid, only sodium phenylbutyrate will dissolve, the excipients will not. The effect of food on sodium phenylbutyrate has not been determined.
Each level teaspoon (enclosed) dispenses 3.2 grams of powder and 3.0 grams of sodium phenylbutyrate. Each level tablespoon (enclosed) dispenses 9.1 grams of powder and 8.6 grams of sodium phenylbutyrate.
Shake lightly before use.
The safety or efficacy of doses in excess of 20 grams (40 tablets) per day has not been established.
NUTRITIONAL MANAGEMENT
To promote growth and development, plasma levels of ammonia, arginine, branched-chain amino acids, and serum protein should be maintained within normal limits while plasma glutamine is maintained at levels less than 1,000 µmol/L. Minimum daily protein intake for a patient of a particular age should be taken from, for example, "Recommended Dietary Allowances", 10th ed., Food and Nutrition Board, National Academy of Sciences, 1989. The allocation of dietary nitrogen into natural protein and essential amino acids is a function of age, residual urea-cycle enzyme activity, and the dose of sodium phenylbutyrate.
At the recommended dose of sodium phenylbutyrate, it is suggested that infants with neonatal-onset CPS and OTC deficiencies initially receive a daily dietary protein intake limited to approximately 1.6 g/kg/day for the first 4 months of life. If tolerated, the daily protein intake may be increased to 1.9 g/kg/day during this period. Protein tolerance will decrease as the growth rate decreases, requiring a reduction in dietary nitrogen intake. From 4 months to 1 year of age, it is recommended that the infant receive at least 1.4 g/kg/day, but 1.7 g/kg/day is advisable. From 1 to 3 years of age, the protein intake should not be less than 1.2 g/kg/day; 1.4 g/kg/day is advisable during this period. For neonatal-onset patients with carbamylphosphate synthetase deficiency or ornithine transcarbamylase deficiency who are at least 6 months of age, it is recommended that the daily protein intake be equally divided between natural protein and supplemental essential amino acids.
Patients with argininosuccinic acid synthetase deficiency and those with late-onset disease (partial deficiencies, including females heterozygous for ornithine transcarbamylase), initially may receive a diet containing the age-determined minimal daily natural protein allowance. The protein intake may be increased as tolerated and determined by plasma glutamine and other amino acid levels. However, many patients with partial deficiencies avoid dietary protein.
Citrulline supplementation is required and recommended for patients diagnosed with neonatal-onset deficiency of carbamylphosphate synthetase or ornithine transcarbamylase; citrulline daily intake is recommended at 0.17 g/kg/day or 3.8 g/m2/day.
The free-base form of arginine may be used instead of citrulline in patients with milder forms of carbamylphosphate synthetase and ornithine transcarbamylase deficiency (daily intake is recommended at 0.17 g/kg/day or 3.8 g/m2/day).
Arginine supplementation is needed for patients diagnosed with deficiency of argininosuccinic acid synthetase; arginine (free base) daily intake is recommended at 0.4 – 0.7 g/kg/day or 8.8 – 15.4 g/m2/day.
If caloric supplementation is indicated, a protein-free product is recommended. Caloric intake should be based upon the "Recommended Dietary Allowances", 10th ed., Food and Nutrition Board, National Research Council, National Academy of Sciences, 1989.
How is Buphenyl Supplied
Buphenyl® Tablets are available in 250 cc bottles which contain 250 sodium phenylbutyrate tablets (NDC 62592-496-03). The bottles are equipped with child-resistant caps. Each tablet is off-white, oval, and embossed with "UCY 500". Each tablet contains 500 mg of sodium phenylbutyrate. STORE AT ROOM TEMPERATURE 15°C – 30°C (59°F – 86°F). AFTER OPENING, KEEP BOTTLE TIGHTLY CLOSED.
Buphenyl® Powder is available in 500 cc bottles, which hold 266 grams of powder, containing 250 grams of sodium phenylbutyrate (NDC 62592-188-64). The bottles are equipped with child-resistant caps. Measurers are provided. Each level teaspoon (enclosed) dispenses 3.2 grams of powder and 3.0 grams of sodium phenylbutyrate. Each level tablespoon (enclosed) dispenses 9.1 grams of powder and 8.6 grams of sodium phenylbutyrate. STORE AT ROOM TEMPERATURE 15°C – 30°C (59°F – 86°F). AFTER OPENING, KEEP BOTTLE TIGHTLY CLOSED.

-----------------------------------------------------------------注：以下产品不同剂型和不同规格，购买时请以电话咨询为准！
-----------------------------------------------------------------原产地英文商品名:
BUPHENYL POWDER 250g/bottle
原产地英文药品名:
SODIUM PHENYLBUTYRATE
中文参考商品译名:
BUPHENYL粉剂 250克/瓶
中文参考药品译名:
苯丁酸钠
生产厂家中文参考译名:
MEDICIS
生产厂家英文名:
MEDICIS

---------------------------------------------------------------
原产地英文商品名:
BUPHENYL TABLET 500mg/tab 250tabs/bottle
原产地英文药品名:
SODIUM PHENYLBUTYRATE
中文参考商品译名:
BUPHENYL片剂 500毫克/片 250片/瓶
中文参考药品译名:
苯丁酸钠
生产厂家中文参考译名:
MEDICIS
生产厂家英文名:
MEDICIS