Disodium edetate

Rising’s Edetate calcium disodium injection is FDA-approved and immediately available Edetate calcium disodium injection is indicated for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. 1 EAST BRUNSWICK, N.J.--(BUSINESS WIRE)-- #adultleadpoisoning --Rising Pharma Holdings, Inc., d/b/a Rising Pharmaceuticals, Inc. (“Rising”) announced commercial availability of Edetate calcium disodium injection. Access to Rising’s product continues despite a commercial shortage of this product in the United States. Rising’s Edetate calcium disodium injection is indicated for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. “Rising’s Edetate calcium disodium injection provides an available option for health care providers to treat patients exposed to lead poisoning,” said David Picard, Executive Vice President for Institutional Markets at Rising. “This continued availability reflects our ongoing commitment to addressing product supply shortages to help ensure health care providers have access to products for patient care.” Edetate Calcium Disodium injection, USP 5 mL single-dose vial containing 200 mg of edetate calcium disodium per mL (1000 mg per vial) Supplied in boxes containing 5 vials (NDC 64980-588-51) Wholesale Item Numbers Cardinal 5855416 Cencora 10291753 Mckesson 2830826 Morris Dickson 296285 ___________________________ 1 Full prescribing information and label available at and provided below. About Rising Pharmaceuticals, Inc. Rising Pharmaceuticals, Inc. is a leading provider of generic and specialty-branded pharmaceuticals in the U.S. Rising focuses on the development, regulatory, and commercial aspects of the product life cycle while outsourcing manufacturing to its network of strategic CMO and CDO partners. With over 182 commercialized generic medicines and over 620 active SKUs, Rising has one of the largest portfolios of any generic pharmaceutical company in the US market. Through an extensive global network of manufacturing facilities, Rising supplies almost 9 billion doses of generic medicine to the market annually. The Company is based in New Brunswick, New Jersey. For more information about the Company, please visit . Edetate Calcium Disodium Injection, USP Intravenous or Intramuscular Use Rx Only WARNINGS Edetate calcium disodium injection is capable of producing toxic effects which can be fatal. Lead encephalopathy is relatively rare in adults, but occurs more often in pediatric patients in whom it may be incipient and thus overlooked. The mortality rate in pediatric patients has been high. Patients with lead encephalopathy and cerebral edema may experience a lethal increase in intracranial pressure following intravenous infusion; the intramuscular route is preferred for these patients. In cases where the intravenous route is necessary, avoid rapid infusion. The dosage schedule should be followed and at no time should the recommended daily dose be exceeded. DESCRIPTION Edetate Calcium Disodium injection, USP is a sterile, injectable, chelating agent in concentrated solution for intravenous infusion or intramuscular injection. Each 5 mL single-dose vial contains 1000 mg of edetate calcium disodium (equivalent to 200 mg/mL) in water for injection and sodium hydroxide (as pH adjuster). Chemically, this product is called [[N,N'-1,2-ethanediyl-bis[N-(carboxymethyl)-glycinato]](4-)-N,N’,O,O’,ON,ON’]-, disodium, hydrate, (OC-6-21)-Calciate(2-). CLINICAL PHARMACOLOGY The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron mobilized are not significant. Copper1 is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased.1 Edetate calcium disodium is poorly absorbed from the gastrointestinal tract. In blood, all the drug is found in the plasma. Edetate calcium disodium does not appear to penetrate cells; it is distributed primarily in the extracellular fluid with only about 5% of the plasma concentration found in spinal fluid. The half life of edetate calcium disodium is 20 to 60 minutes. It is excreted primarily by the kidney, with about 50% excreted in one hour and over 95% within 24 hours.2 Almost none of the compound is metabolized. The primary source of lead chelated by edetate calcium disodium is from bone; subsequently, soft-tissue lead is redistributed to bone when chelation is stopped.3,4 There is also some reduction in kidney lead levels following chelation therapy. It has been shown in animals that following a single dose of edetate calcium disodium urinary lead output increases, blood lead concentration decreases, but brain lead is significantly increased due to internal redistribution of lead.5 (See WARNINGS .) These data are in agreement with the recent results of others in experimental animals showing that after a five day course of treatment there is no net reduction in brain lead.6 INDICATIONS AND USAGE Edetate calcium disodium injection is indicated for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. Chelation therapy should not replace effective measures to eliminate or reduce further exposure to lead. CONTRAINDICATIONS Edetate calcium disodium injection should not be given during periods of anuria, nor to patients with active renal disease or hepatitis. WARNINGS See boxed warning . PRECAUTIONS General Precautions Edetate calcium disodium may produce the same renal damage as lead poisoning, such as proteinuria and microscopic hematuria. Treatment-induced nephrotoxicity is dose-dependent and may be reduced by assuring adequate diuresis before therapy begins. Urine flow must be monitored throughout therapy which must be stopped if anuria or severe oliguria develop. The proximal tubule hydropic degeneration usually recovers upon cessation of therapy. Edetate calcium disodium must be used in reduced doses in patients with pre-existing mild renal disease. Patients should be monitored for cardiac rhythm irregularities and other ECG changes during intravenous therapy. Information for patients Patients should be instructed to immediately inform their physician if urine output stops for a period of 12 hours. Laboratory tests Urinalysis and urine sediment, renal and hepatic function and serum electrolyte levels should be checked before each course of therapy and then be monitored daily during therapy in severe cases, and in less serious cases after the second and fifth day of therapy. Therapy must be discontinued at the first sign of renal toxicity. The presence of large renal epithelial cells or increasing number of red blood cells in urinary sediment or greater proteinuria call for immediate stopping of edetate calcium disodium administration. Alkaline phosphatase values are frequently depressed (possibly due to decreased serum zinc levels), but return to normal within 48 hours after cessation of therapy. Elevated erythrocyte protoporphyrin levels (> 35 mcg/dl of whole blood) indicate the need to perform a venous blood lead determination. If the whole blood lead concentration is between 25 to 55 mcg/dl a mobilization test can be considered.7,8 (See Diagnostic Test .) An elevation of urinary coproporphyrin (adults: > 250 mcg/day; pediatric patients under 80 lbs: > 75 mcg/day) and elevation of urinary delta aminolevulinic acid (ALA) (adults: > 4 mg/day; pediatric patients: > 3 mg/m2/day) are associated with blood lead levels > 40 mcg/dl. Urinary coproporphyrin may be falsely negative in terminal patients and in severely iron-depleted pediatric patients who are not regenerating heme.9 In growing pediatric patients long bone x-rays showing lead lines and abdominal x-rays showing radio-opaque material in the abdomen may be of help in estimating the level of exposure to lead. Drug Interactions There is no known drug interference with standard clinical laboratory tests. Steroids enhance the renal toxicity of edetate calcium disodium in animals.7 Edetate calcium disodium interferes with the action of zinc insulin preparations by chelating the zinc.7 Carcinogenesis, Mutagenesis, Impairment of Fertility Long term animal studies have not been conducted with edetate calcium disodium to evaluate its carcinogenic potential, mutagenic potential or its effect on fertility. Pregnancy Category B One reproduction study was performed in rats at doses up to 13 times the human dose and revealed no evidence of impaired fertility or harm to the fetus due to edetate calcium disodium.10 Another reproduction study performed in rats at doses up to about 25 to 40 times the human dose revealed evidence of fetal malformations due to edetate calcium disodium, which were prevented by simultaneous supplementation of dietary zinc.11 There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed. Labor and Delivery Edetate calcium disodium has no recognized use during labor and delivery, and its effects during these processes are unknown. 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 edetate calcium disodium is administered to a nursing woman. Pediatric Use Since lead poisoning occurs in pediatric populations and adults but is frequently more severe in pediatric patients, edetate calcium disodium is used in patients of all ages. The intramuscular route is preferred by some for young pediatric patients. In cases where the intravenous route is necessary, avoid rapid infusion. (See WARNINGS .) Urine flow must be monitored throughout therapy; Edetate Calcium Disodium therapy must be stopped if anuria or severe oliguria develops. (See General Precautions .) At no time should the recommended daily dosage be exceeded. (See DOSAGE AND ADMINISTRATION .) ADVERSE REACTIONS The following adverse effects have been associated with the use of edetate calcium disodium: Body as a Whole: pain at intramuscular injection site, fever, chills, malaise, fatigue, myalgia, arthralgia. Cardiovascular: hypotension, cardiac rhythm irregularities. Renal: acute necrosis of proximal tubules (which may result in fatal nephrosis), infrequent changes in distal tubules and glomeruli. Urinary: glycosuria, proteinuria, microscopic hematuria and large epithelial cells in urinary sediment. Nervous System: tremors, headache, numbness, tingling. Gastrointestinal: cheilosis, nausea, vomiting, anorexia, excessive thirst. Hepatic: mild increases in SGOT and SGPT are common, and return to normal within 48 hours after cessation of therapy. Immunogenic: histamine-like reactions (sneezing, nasal congestion, lacrimation), rash. Hematopoietic: transient bone marrow depression, anemia. Metabolic: zinc deficiency, hypercalcemia. To report SUSPECTED ADVERSE REACTIONS, contact Rising Pharma Holdings, Inc. at 1-844-874-7464 or FDA at 1-800-FDA-1088 or . OVERDOSAGE Symptoms Inadvertent administration of 5 times the recommended dose, infused intravenously over a 24 hour period, to an asymptomatic 16 month old patient with a blood lead content of 56 mcg/dl did not cause any ill effects. Edetate calcium disodium can aggravate the symptoms of severe lead poisoning, therefore, most toxic effects (cerebral edema, renal tubular necrosis) appear to be associated with lead poisoning. Because of cerebral edema, a therapeutic dose may be lethal to an adult or a pediatric patient with lead encephalopathy. Higher dosage of edetate calcium disodium may produce a more severe zinc deficiency. Treatment Cerebral edema should be treated with repeated doses of mannitol. Steroids enhance the renal toxicity of edetate calcium disodium in animals and, therefore, are no longer recommended.7 Zinc levels must be monitored. Good urinary output must be maintained because diuresis will enhance drug elimination. It is not known if edetate calcium disodium is dialyzable. DOSAGE AND ADMINISTRATION When a source for the lead intoxication has been identified, the patient should be removed from the source, if possible. The recommended dose of edetate calcium disodium for asymptomatic adults and pediatric patients whose blood lead level is 20 mcg/dl (World Health Organization recommended upper allowable level) is 1000 mg/m2/day whether given intravenously or intramuscularly. (See Surface Area Nomogram.) For adults with lead nephropathy, the following dosing regimen has been suggested: 500 mg/m2 every 24 hours for 5 days for patients with serum creatinine levels of 2 to 3 mg/dl, every 48 hours for 3 doses for patients with creatinine levels of 3 to 4 mg/dl, and once weekly for patients with creatinine levels above 4 mg/dl. These regimens may be repeated at one month intervals.12 Edetate calcium disodium, used alone, may aggravate symptoms in patients with very high blood lead levels. When the blood lead level is > 70 mcg/dl or clinical symptoms consistent with lead poisoning are present, it is recommended that edetate calcium disodium be used in conjunction with BAL (dimercaprol). Please consult published protocols and specialized references for dosage recommendations of combination therapy.14-18 Therapy of lead poisoning in adults and pediatric patients with edetate calcium disodium is continued over a period of five days. Therapy is then interrupted for 2 to 4 days to allow redistribution of the lead and to prevent severe depletion of zinc and other essential metals. Two courses of treatment are usually employed; however, it depends on severity of the lead toxicity and the patient’s tolerance of the drug. Edetate calcium disodium is equally effective whether administered intravenously or intramuscularly. The intramuscular route is used for all patients with overt lead encephalopathy and this route is preferred by some for young pediatric patients. Acutely ill individuals may be dehydrated from vomiting. Since edetate calcium disodium is excreted almost exclusively in the urine, it is very important to establish urine flow with intravenous fluid administration before the first dose of the chelating agent is given; however, excessive fluid must be avoided in patients with encephalopathy. Once urine flow is established, further intravenous fluid is restricted to basal water and electrolyte requirements. Administration of edetate calcium disodium should be stopped whenever there is cessation of urine flow in order to avoid unduly high tissue levels of the drug. Edetate calcium disodium must be used in reduced doses in patients with pre-existing mild renal disease. Intravenous Administration Add the total daily dose of edetate calcium disodium (1000 mg/m2/day) to 250-500 mL of 5% dextrose or 0.9% sodium chloride injection. The total daily dose should be infused over a period of 8 to 12 hours. Discard unused portion. Edetate calcium disodium injection is incompatible with 10% dextrose, 10% invert sugar in 0.9% sodium chloride, lactate Ringer’s, Ringer’s, one-sixth molar sodium lactate injections, and with injectable amphotericin B and hydralazine hydrochloride. Intramuscular Administration The total daily dosage (1000 mg/m2/day) should be divided into equal doses spaced 8 to 12 hours apart. Discard unused portion. Lidocaine or procaine should be added to the edetate calcium disodium injection to minimize pain at the injection site. The final lidocaine or procaine concentration of 5 mg/mL (0.5%) can be obtained as follows: 0.25 mL of 10% lidocaine solution per 5 mL concentrated edetate calcium disodium; 1 mL of 1% lidocaine or procaine solution per mL of concentrated edetate calcium disodium. When used alone, regardless of method of administration, edetate calcium disodium should not be given at doses larger than those recommended. Diagnostic Test Several methods have been described for lead mobilization tests using edetate calcium disodium to assess body stores.7, 9,12,13,18 These procedures have advantages and disadvantages that should be reviewed in current references. Edetate calcium disodium mobilization tests should not be performed in symptomatic patients and in patients with blood lead levels above 55 mcg/dl for whom appropriate therapy is indicated. Parenteral drugs should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. HOW SUPPLIED Edetate Calcium Disodium injection, USP 5 mL single-dose vial (NDC 64980-588-05 ) containing 200 mg of edetate calcium disodium per mL (1000 mg per vial), in boxes containing 5 vials (NDC 64980-588-51 ). Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature]. Rx Only This product is non-returnable. REFERENCES 1. Thomas DJ, Chisolm JJ. Lead, zinc and copper decorporation during calcium disodium ethylene diamine tetraacetate treatment of lead-poisoned children. J Pharmacol Exp Therapeu 1986; 239: 829–835. 2. The Pharmacological Basis of Therapeutics, 7th edition, Goodman and Gilman, editors. MacMillan Publishing Company, New York, 1985, pp. 1619–1622. 3. Hammond PB, Aronson AL, Olson WC. The mechanism of mobilization of lead by ethylenediaminetetraacetate. J Pharmacol Exp Therapeu 1967; 157: 196–206. 4. Van deVyver FL, D’Haese PC, Visser WJ, et al. Bone lead in dialysis patients. Kidney Intl 1988; 33: 601–607. 5. Cory-Slecta DA, Weiss B, Cox C. Mobilization and redistribution of lead over the course of calcium disodium ethylene diamine tetraacetate chelation therapy. J Pharmacol Exp Therapeu 1987; 243: 804–813. 6. Chisolm JJ. Mobilization of lead by calcium disodium edetate. Am J Dis Child 1987;141: 1256–1257. 7. Drug Evaluations, 6th Edition, American Medical Association, Saunders, Philadelphia, 1986, pp. 1637–1639. 8. Centers for Disease Control: Preventing lead poisoning in young children. Atlanta, GA, Department of Health and Human Services, 1985 Jan. 9. Finberg L, Rajagopal V. Diagnosis and treatment of lead poisoning in children. J Family Med 1985 April: 3–12. 10. Schardein JL, Sakowski R, Petrere J, et al. Teratogenesis studies with EDTA and its salts in rats. Toxicol Appl Pharmacol 1981; 61: 423–428. 11. Swenerton H, Hurley LS. Teratogenic effects of a chelating agent and their prevention by zinc. Science 1971; 173: 62–64. 12. American Hospital Formulary Service, Drug Information, 1988, pp. 1695–1698. 13. Markowitz ME, Rosen JF. Assessment of lead stores in children: Validation of an 8-hour CaNa2EDTA (Edetate Calcium Disodium) provocative test. J Pediatrics 1984;104: 337–341. 14. Piomelli S, Rosen JF, Chisolm JJ, et al. Management of childhood lead poisoning. J Pediatrics 1984; 105: 523–532. 15. Sachs HK, Blanksma LA, Murray EF, et al. Ambulatory treatment of lead poisoning: Report of 1,155 cases. Pediatrics 1970; 46: 389. 16. Chisolm JJ. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatrics 1968; 73: 1. 17. Coffin R, Phillips JL, Staples WI, et al. Treatment of lead encephalopathy in children. J Pediatrics 1966; 69: 198–206. 18. Chisolm JJ. Increased lead absorption and acute lead poisoning. Current Pediatric Therapy 12, Gillis and Kagan, editors, WB Saunders, Philadelphia, 1986, pp. 667–671. Distributed by: Rising Pharma Holdings, Inc. East Brunswick, NJ 08816. Made in India Contacts For Media Inquiries: Marina Wissa, (201) 961 9013 mediainquiries@risingpharma.com For Customer Service Inquiries: Jason Eisner, (201) 961 9000 customerservice@risingpharma.com

✦ ✦ ✦ 随着中国经济的快速增长和科技实力的提升，国内新药研发蓬勃发展，为出海打下良好基础。一直以来，中国医药、原料药出口贸易在东南亚市场占有举足轻重的份额。其中，印度尼西亚、泰国、越南、菲律宾和马来西亚五个国家占据了东南亚医药市场的90%以上。未来这些国家将会成为国内企业转战的重要市场，包括投资建厂等深度合作开发。 为助力中国药企加速布局东南亚医药市场，9月11日，东南亚医药市场开拓机遇与挑战主题会议将于CPHI & PMEC 制药工业展（深圳）展会期间在深圳会展中心（福田）举办。会议将从当下市场的最新国际形势出发，结合案例与报告，与上下游企业共同探讨东南亚市场的发展机遇。 ✦ ✦ ✦ 东南亚医药市场开拓机遇与挑战主题会议 会议时间 9月11日 会议地点 深圳会展中心（福田） 论坛区A（展位：9A56） 主办单位 上海博华国际展览有限公司 承办单位 北京东方比特科技有限公司 协办单位 E药经理人 扫描太阳码 0元领票并报名听会 8月30日前完成预登记 现场可领取电子会刊一份 SHENZHEN 会议议程 09:30 主持人致辞 09:40-10:20  东南亚国家医药国际贸易报告 嘉宾介绍 吴惠芳 北京东方比特（健康网）总经理兼首席研究员，北京玉德未来控股有限公司副总裁 吴女士在军事医学科学院药物分析专业获理学硕士学位，1980年起从事药学相关工作，2000年前在部队医疗、科研机构从事临床药学、科研管理等工作，技术职务副主任药师。2000年退役后从事医药信息研究工作，专注于医药行业研究、市场研究、产业链结构研究等领域。在医药原料药、医药商品进出口、医药产业数据等信息方面有发布了大量文献资料和报告发表。为国内外企业、政府和科研机构提供咨询服务。连续多年为“中国化学制药工业协会”所著《医药发展蓝皮书》、《中国医药手册》作者之一；是《中国医药报》、《医药经济报》的特约撰稿人，在国内重要医药报刊发表大量文章。多次被邀请在中国医药行业大型会议和展览上做有关中国医药市场专题演讲。她的演讲以实际数据和案例阐明问题、总结变化规律，在中国制药企业中广为流传，受到医药界的好评。 ☝🏿☝🏿上下滑动了解嘉宾完整简介 10:20-10:50  中国制药企业出海东南亚国家的案例分享 嘉宾介绍 王亚锋 上海医药国际业务事业部东南亚区域负责人、上药泰国总经理 中国药科大学本科，中欧国际工商学院Global EMBA。 从事医药国际营销工作十余年，深厚的医药行业知识和专业能力。拥有丰富的海外子公司运营和营销团队管理经验。深度参与海外工厂立项，写字楼，仓库等绿地项目建设。 海外常驻包括非洲加纳，尼日利亚，乌干达，科特迪瓦，东南亚泰国，菲律宾等多个国家。熟悉多个市场药政法规以及行业准入要求。多次在海外国家从零开始设立全资公司、合资公司，组建销售团队，实现业绩从零突破，运作药品进入国家用药指南和国家医保。所在团队曾实现单品种中国制剂出口第一。 历任复星医药集团桂林南药国际商务代表，销售经理，海外国家经理，大区经理等，现任上海医药国际业务事业部东南亚区域负责人，上药泰国总经理。 ☝🏿☝🏿上下滑动了解嘉宾完整简介 10:50-11:20  印度尼西亚制药业的机遇和市场开拓实践 嘉宾介绍 张君丽 成都市一诺医药化工有限公司总经理采购总监 公司团队深耕印尼市场十年，专注医药API等产品出口； 聘请多名印尼本地员工，长期穿梭在印尼各个制剂工厂，拜访客户，与当地前十大药企均有超级深度的合作与链接！ 11:20-11:45  印尼清真医药产品市场情况更新 嘉宾介绍 Dr. Ir. Muslich, M.Si Halal Partnership  and Audit Services Director, LPPOM 获得IPB大学学士(S1)、研究生(S2)和博士(S3)学位;此前曾在多家私营公司工作(1991年至1993年)，PT TELKOM WITEL IX Jayapura农业和农用工业发展中心经理(1993年至1994年)，LPPOM MUI清真保证体系负责人(2010年至2015年)，QA和LPPOM MUI标准负责人(2015年至2019年)，LPPOM MUI高级顾问(2020年)，MUI清真认证要求开发团队负责人(2010年至2011年);现为IPB大学农业技术学院农业工业工程系讲师(自1994年起)，清真审核员(自1995年起)，清真管理体系标准制定技术委员会(SNI 99 001)成员，清真家禽屠宰场(SNI 99 002)，家庭切清真反刍(SNI 99 003)，清真食品(SNI 99 004)国家标准化机构(自2015年起)，SKKNI主管能力测试设备开发团队负责人Halal & SKKNI清真审核员(自2017年起)，国家认证机构能力评估员职业(BNSP)(自2015年起)，食品安全能力评估员，机构专业认证(LSP)食品质量保证与安全(JMKP)(自2015年起);于2020-2022年被任命为LPPOM MUI清真合作与审计服务总监。 ☝🏿☝🏿上下滑动了解嘉宾完整简介 11:20-12:00  圆桌讨论：寻找东南亚市场的机会 讨论嘉宾 深圳市远邦医药有限公司 湖南尔康制药股份有限公司 成都倍特药业有限公司 广州康臣药业有限公司 ...... 扫描太阳码 0元领票并报名听会 8月30日前完成预登记 现场可领取电子会刊一份 把握东南亚市场发展机遇 加速融入全球制药供应链 随着东南亚医药市场的发展潜能进一步释放，中国医药企业将迎来更多发展机遇。作为中国药企链接国际市场的重要纽带，CPHI & PMEC 制药工业展（深圳）将携手400余家优质展商，共同探索企业在东南亚乃至全球市场的发展路径。 下面就请跟随小编的步伐，一起走近本期的优选展商吧！ 浙江瑞邦药业股份有限公司 展位：9F08 浙江瑞邦药业股份有限公司成立于1956年，具有60多年生产医药原料药和食品添加剂的生产经验。公司以药品生产质量管理规范（GMP) 标准组织生产和销售。本公司的产品获得了美国FDA，欧洲CEP和中国GMP的认证。主要产品有葡萄糖酸盐系列，莫匹罗星，莫匹罗星钙，环孢菌素，夫西地酸等。浙江瑞邦药业股份有限公司在国内外都享有良好的声誉。产品远销美国，欧洲，日本，印度及其他南美和东南亚地区。 主推产品 环孢菌素、莫匹罗星、莫匹罗星钙、葡萄糖酸钙、葡萄糖酸锌、葡萄糖酸钾、葡萄糖酸镁、葡萄糖酸亚铁、葡萄糖酸铜、葡萄糖酸锰、葡萄糖酸钠、多粘菌素B、夫西地酸、夫西地酸钠、米尔贝肟、葡萄糖酸内酯、非达霉素、甘草次酸、原儿茶酸。 ☝🏿☝🏿上下滑动查看完整展商介绍 河北华晨药业集团有限公司 展位：9D46 河北华晨药业集团有限公司，始建于1991年，坐落于黄骅经济开发区。是一家集研发、生产、销售药用包装材料、原料药、制剂、医疗器械，开展国内外贸易为一体的医药企业。集团公司现下设河北华晨药业有限公司、黄骅华宾生物科技有限公司、河北华迪药业有限公司、华晨吉海（北京）药物研究院。目前华晨药业拥有通过GMP认证的药用氯化钠、碳酸氢钠、氯化钾及新增制剂包括片剂、硬胶囊制剂、颗粒剂、散剂、软膏剂、凝胶贴膏剂、口服液等数十种，同时生产药用PE袋、膜、包装桶、瓶等药用包装材料等。 主推产品 氯化钠、碳酸氢钠、氯化钾、氯化钙、氯化铵、依地酸二钠、重酒石酸胆碱、富马酸（辅料、富马酸亚铁、醋酸钙、醋酸钠、硫酸镁、碘化钾、氯化镁、富马酸亚铁、葡萄糖酸锌、葡萄糖二酸钙、双乙酸钠、树脂再生剂、碳酸镧、硫酸钾、利多卡因、氟比洛芬、氯化镁、麝香草粉、盐酸利多卡因、葡萄糖酸钙、洛索洛芬钠、磷酸奥司他韦、无水硫酸钠、氨苯蝶啶、托匹司特、硫酸亚铁、西甲硅油、硫酸双肼屈嗪、甘羟鋁、葡萄糖酸亚铁、叔丁醇镁、异丙醇镁、二甲硅油、碳酸钙、亚硫酸镁（六水）、硫酸钾、乳酸钙、乳酸钠、乳果糖、丙胺卡因、喷托维林、丁卡因、双氯芬酸依泊胺、克立硼罗、阿达帕林、盐酸异丙嗪、高岭土、克罗米通、盐酸异丙嗪、氨苯蝶啶、叔丁醇镁、异丙醇镁、亚硫酸镁知名。 ☝🏿☝🏿上下滑动查看完整展商介绍 山西阳和药业有限公司 展位号：9A13 山西阳和药业有限公司成立于2017年，坐落于山西省大同市阳高县龙泉工业园区。公司注册资本5100万元，总占地面积100亩。阳和药业作为化学原料药的商业化生产基地，专业从事特色化学原料药的研发、生产、销售。公司现拥有多条原料药生产线，产品涉及呼吸系统、消化系统等多个领域。目前公司可大批量生产乙酰半胱氨酸、间苯三酚、间苯三酚三甲醚、聚乙烯醇等原料药。 主推产品 乙酰半胱氨酸、间苯三酚、聚乙烯醇、间苯三酚三甲醚。 ☝🏿☝🏿上下滑动查看完整展商介绍 浙江荣耀生物科技股份有限公司 展位：9C51 浙江荣耀生物科技股份有限公司创立于1999年，位于台州湾经济技术开发区，是一家集研发、生产、销售于一体的创新型医药企业，是国家高新技术企业、浙江省专精特新中小企业、浙江省科技型中小企业。业务涵盖医药原料药及中间体、兽药原料药及中间体、CDMO等。 主推产品 二硝托胺148-01-6、甲砜霉素15318-45-3、氟苯尼考73231-34-2、非班太尔58306-30-2、芬苯达唑43210-67-9、莫昔克丁113507-06-5、赛拉菌素220119-17-5、氟雷拉纳864731-61-3、奥拉替尼1208319-26-9、2-氨基-N-(2、2、2-三氟乙基)乙酰胺盐酸盐1171331-39-7、三氯苯达唑68786-66-3、癸氧喹酯18507-89-6、尼卡巴嗪330-95-0、3′、5′-二氯-2、2、2-三氟苯乙酮130336-16-2、4-氯吡咯并嘧啶3680-69-1、反式-N-甲基-[4-(甲氨基)环己基]甲磺酰胺1809995-95-6、依帕司他82159-09-9、盐酸氨溴索23828-92-4、盐酸金刚乙胺1501-84-4、盐酸溴己新611-75-6、西司他丁82009-34-5、3-甲基-6-硝基-1H-吲唑6494-19-5、2-[4-(2-吡啶基)苄基]-肼羧酸叔丁酯198904-85-7、2-氨基-1-(2、5-二甲氧基苯基)乙醇3600-87-1、3-(三氟甲基)-5、6、7、8-四氢-[1、2、4]三唑并[4、3-a]吡嗪盐酸盐762240-92-6、(3S、4R)-4-(4-氟苯基)-1-甲基-3-哌啶甲醇105812-81-5、1-(4-氨基苯基)环戊甲腈115279-73-7、3-氨基-1-金刚烷醇702-82-9、1-金刚烷甲酸828-51-3、2-金刚烷酮700-58-3、1-金刚烷胺768-94-5、1-金刚烷甲醇770-71-8、2-金刚烷醇700-57-2、1-金刚烷醇768-95-6。 ☝🏿☝🏿上下滑动查看完整展商介绍 江苏宇田医药有限公司 展位：9E31 江苏宇田医药有限公司是一家从事现代医药研发、生产、销售为一体的新型特色API及CDMO制药企业，致力于为国内各大制药企业提供高质量的原料药与中间体，公司产品同时远销欧洲、日韩、印度等数十个国家，为国家重点高新技术企业、市科技小巨人企业、中华药港新医药产业基地骨干企业之一。 宇田医药始终把科研开发作为企业可持续发展的支撑力量，是国内科研投入较多的药企之一，公司以连云港研发中心为科研载体，配合杭州科巢生物科技、连云港万科生物科技、黑龙江迪诺医药，自主创新能力不断增强。形成了“以一带三”的良性格局。宇田医药在江苏连云港、黑龙江佳木斯建有两个生产基地，获得国家高新技术企业、省级工程技术研究中心、江苏省瞪羚企业、江苏省科技型中小企业、安全标准化二级企业、省两化融合示范试点企业，同时也获得了原料药品种的GMP和注册现场核查的二合一认证，先后承担省/市级成果转换等多个省/市级科技项目；获得授权专利与商标数十项；通过ISO9000、ISO14000认证。这些荣誉的取得标志着企业药品生产质量和管理水平走在了全国医药行业前列。 主推产品 原料药：碘克沙醇、碘海醇、阿托伐他汀钙、瑞舒伐他汀钙、盐酸伊伐布雷定、利奈唑胺、西洛多辛、盐酸厄洛替尼、盐酸莫西沙星及各中间体。 中间体：造影剂系列中间体、多尼培南侧链、比阿培南侧链、1,4-丁二磺酸。 ☝🏿☝🏿上下滑动查看完整展商介绍 江苏同禾药业有限公司 展位：9D26 江苏同禾药业有限公司是江苏万兴创业投资有限公司的全资子公司，是一家集制剂药、原料药和保健食品的研发、生产、销售为一体的国家高新技术企业。连续8年，跻身于常熟市百强企业前50 名。 公司拥有原料药、片剂、胶囊剂和颗粒剂的GMP证书。硫辛酸、6.8-二氯辛酸乙酯、右旋硫辛酸钠、环丙贝特、10-甲氧基亚氨基芪等多个产品被评为江苏省高新技术产品；硫辛酸、盐酸二甲双胍等取得了原料药品批件，厄多司坦片、氨酚伪麻分散片和新雪胶囊等取得药品注册批件和新药证书；硫辛酸片和胶囊即将取得新药证书，另有10多个新药正在SFDA审批中。调节血糖和控制并发症的保健食品唐苹片正在全国热销中。 主推产品 硫辛酸系列、右旋硫辛酸、右旋硫辛酸钠盐、右旋硫辛酸氨基丁三醇盐。 ☝🏿☝🏿上下滑动查看完整展商介绍 CPHI & PMEC 制药工业展（深圳）致力于打造国际化制药产业生态圈，汇集产业链上下游实力企业，以技术驱动产业提升，助推更多中国药企扬帆“出海”，聚势共赢！ 扫描二维码 0元领票 8月30日前完成预登记 现场可领取电子会刊一份 金秋九月·不见不散！ 联系我们 参观咨询 林女士 电话：021-33392105 邮箱：ashley.lin@imsinoexpo.com 张女士 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