Dequalinium Chloride

河北牵头的京津冀联盟集采和河北省集采，备受关注，原因有两个： 一是规则简单粗暴，最低价或次低价中标，独家品种必须满足特定降幅； 二是产品亮眼，很多是临床用量特别大的独家品种。 因此，标书发布后，几人欢喜多家愁。喜的是少数光脚企业，只要能狠下心降价，就有机会抢市场； 愁的是现有市场主导者，面临巨大挑战，还有很多独家品种，也在纠结要不要降价中标，现在全国价格一盘棋，牵一发动全身，河北降，全国就得降。 我之前整理了个产品的市场竞争格局，今天补充京津冀集采产品市场销售规模数据，大家可以通过数据，判断每个品种竞争态势，筛选产品机会。 举几个例子： 雷尼替丁注射剂，销售额6千多万，厂家较多，头部3个企业占了主要市场，且价格较高，如果有企业愿意降价，就能很快抢到市场。 乙酰半胱氨酸吸入剂，赞邦和海南斯达两家霸占市场，现在已有多家企业过评，大家都是光脚的，有机会快速抢市场。 山莨菪碱注射剂，成都第一制药独占，这次是否会被低价赶跑。 地佐辛注射剂，扬子江占九成，另一家是否会赌一把。 具体品种情况，大家结合我的数据，认真研究。 京津冀集采品种竞争格局和市场规模情况品种名称剂型同组企业数 市场规模（千万 元）市场份额TOP2苯唑西林注射剂204石药中诺30%，苏州二叶26%雷尼替丁注射剂286安徽长江39%，现代哈森30%乙酰半胱氨酸吸入用溶液剂2920赞邦51%，海南斯达38%溴己新注射剂286石家庄四药66%，一品红34%纳布啡注射剂45宜昌人福60%，扬子江36%布托啡诺注射剂49恒瑞99%依西美坦口服常释剂型815辉瑞95%，齐鲁4%(消旋)山莨菪碱注射剂472.7成都第一98%乳果糖口服液体剂2711雅培65%，韩美20%玻璃酸钠注射剂64.3生化学54%，昊海26%复方利血平氨苯蝶啶口服常释剂型2大蒜素注射剂710辰欣100%尿素[13C]呼气试验药盒、验药盒、诊断试剂盒52.6华亘安邦70%，海德润30%万古霉素注射剂717VANCOCIN81%，浙江医药10%地佐辛注射剂218扬子江91%，南京优科9%吡拉西坦口服常释剂型4001.2江西亿友76%，吉林双药7%喷他佐辛注射剂36华润双鹤100%普萘洛尔注射剂32.3朗欧100%羧甲司坦口服液体剂118北京诚济97%米那普仑口服常释剂型42上海现代100%琥珀酸亚铁口服常释剂型53.5金陵药业87%，成都地奥10%表柔比星注射剂83.3辉瑞80%，瀚晖11%阿戈美拉汀口服常释剂型86豪森82%，施维雅18%劳拉西泮口服常释剂型52大西洋43%，湖南洞庭38%戊乙奎醚注射剂61.3锦州奥鸿88%，恩华11%磷霉素氨丁三醇口服散剂36山西仟源62%，沈阳第一24%双氯芬酸钠缓释控释剂型23非诺贝特口服常释剂型723雅培95%帕利哌酮缓释控释剂型62豪森53%，强生47%中/长链脂肪乳(C6-24)注射剂71.4费森尤斯卡比64%，20%尼卡地平注射剂143安斯泰来93%，成都苑东4%贝尼地平口服常释剂型47协和发酵57%，山东华素43%碘美普尔注射剂37博莱科100%灭菌注射用水(500ml)注射剂442华仁40%，石药银湖22%钆喷酸葡胺注射剂54拜耳45%，北陆42%福莫特罗吸入用溶液8维拉帕米注射剂111.4上海禾丰100%羟乙基淀粉130/0.4电解质注射剂21湖南科伦100%普拉洛芬滴眼剂153日本千寿90%，山东海山8%奈达铂注射剂42吉林金恒47%，奥赛康38%丁螺环酮口服常释剂型4尼可刹米注射剂292瑞阳93%地奈德软膏剂5呋塞米口服常释剂型43他克莫司软膏剂156丹麦利奥85%，四川明欣8%加兰他敏注射剂62.5湖北民康95%绒促性素注射剂172.5丽珠50%，默克44%布美他尼口服常释剂型26地氯雷他定口服液体剂26硝酸异山梨酯口服常释剂型56阿莫西林/克拉维酸钾口服液体剂13夫西地酸软膏剂62香港澳美75%，丹麦利奥24%复方头孢克洛(克洛己新)口服液体剂2胰岛素注射剂11复方氨基酸(15)双肽(2)注射剂34科伦100%奥沙利铂甘露醇注射剂37美大康70%，辰欣30%肠内营养剂(TPF-D)口服液体剂27费森尤斯82%，雅培18%伊托必利口服常释剂型151雅培86%，迪沙13%氨酚羟考酮口服常释剂型35马林克罗88%，华泰晨光12%去氧肾上腺素注射剂93上海禾丰97%螺内酯口服常释剂型36异烟肼注射剂211.4信合68%，西南16%贝达喹啉口服常释剂型33.4强生100%卢帕他定口服常释剂型10培唑帕尼口服常释剂型41.5诺华95%维生素D2注射剂3替加氟栓剂6地诺孕素口服常释剂型77Jennapham98%地喹氯铵含片4班布特罗口服液体剂21岳阳新华达65%，南京海鲸35%头孢克洛缓释控释剂型65苏州西克罗35%，天津中央23%布洛芬口服液体剂1.3强生85%，新华制药6%右美沙芬愈创甘油醚(复方氢溴酸右美沙芬)口服液体剂54.5湖北凤凰白云山89%，南京海鲸6%氨溴特罗口服液体剂191韩美100%拉莫三嗪口服常释剂型82.4葛兰素史克94%佐匹克隆口服常释剂型84齐鲁33%，华润顺峰30%替考拉宁注射剂74浙江医药51%，赛诺菲49%环磷酰胺注射剂51.2百特75%，恒瑞20%利多卡因凝胶剂3氟伐他汀缓释控释剂型33瀚晖62%，北京诺华38%赖氨匹林注射剂221.5通用45%，美好西林20%脂肪乳(C14-24)注射剂191费森尤斯84%，力邦15%苯溴马隆口服常释剂型62Heumann83%，东阳光8%乌拉地尔缓释控释剂型4氨磷汀注射剂41美罗100%七叶皂苷钠注射剂171.2绿叶54%，爱民40%辅酶A注射剂26 数据来源：摩熵医药样本医院市场药品销售数据 市场规模数据来自2023年京津冀地区样本医院销售总额，单位千万元； 未统计低于千万元的产品 相关阅读： 简单粗暴的河北集采，有3类机会 河北集采简单粗暴，最多两家中选，地佐辛、谷红等大品种在列 已经购买“摩熵药筛”小程序全库正式年度会员朋友，可以直接联系客服，获取原始数据。 先用”摩熵药筛“小程序，可以查询产品的竞争、价格、市场销售数据。

Researchers report that, in laboratory cultures and animal models, a drug significantly reduces the ability of bacteria to develop antibiotic resistance, which might prolong antibiotic effectiveness. A team of researchers at Baylor College of Medicine is gaining ground in their search for solutions to the global problem of bacterial antibiotic resistance, which was responsible for nearly 1.3 million deaths in 2019. The team reports in the journal Science Advances a drug that, in laboratory cultures and animal models, significantly reduces the ability of bacteria to develop antibiotic resistance, which might prolong antibiotic effectiveness. The drug, called dequalinium chloride (DEQ), is a proof-of-concept for evolution-slowing drugs. "Most people with bacterial infections get better after completing antibiotic treatment, but there are also many cases in which people decline because the bacteria develop resistance to the antibiotic, which then can no longer kill the bacteria," said corresponding author Dr. Susan M. Rosenberg, Ben F. Love Chair in Cancer Research and professor of molecular and human genetics, biochemistry and molecular biology and molecular virology and microbiology at Baylor. She also is a program leader in Baylor's Dan L Duncan Comprehensive Cancer Center (DLDCCC). In this study, Rosenberg and her colleagues looked for drugs that could prevent or slow down E. coli bacteria from developing resistance to two antibiotics when exposed to a third antibiotic, ciprofloxacin (cipro), the second most prescribed antibiotic in the U.S. and one associated with high bacterial resistance rates. The resistance is caused by new gene mutations that occur in the bacteria during infection. The drug DEQ reduces the speed at which new mutations are formed in bacteria, the team finds. Previous work from the Rosenberg lab had shown that bacterial cultures in the lab exposed to cipro turn up mutation rate. They found a mutational "program" that is switched on by bacterial stress responses. Stress responses are genetic programs that instruct cells to increase production of protective molecules during stress, including stress from low concentrations of cipro. Low concentrations occur at the beginning and end of antibiotic therapies and if doses are missed. The same stress responses also increase the ability to make genetic mutations, the Rosenberg group, then many other labs, have shown. Some of the mutations can confer resistance to cipro, while other mutations can allow resistance to antibiotics not yet encountered. Mutation-generating processes that are turned on by stress responses are called stress-induced mutation mechanisms. Bacteria with antibiotic resistance mutations can then sustain an infection in the presence of cipro. This study is the first to show that in animal infections treated with cipro, the bacteria activate a known stress-induced genetic mutational process. Cipro resistance occurs mostly by the bacteria developing new mutations, both clinically and in the laboratory, rather than by acquiring genes that confer antibiotic resistance from other bacteria. Looking to prevent the development of antibiotic resistance, the researchers screened 1,120 drugs approved for human use for their ability to dial down the master bacterial stress response, which they showed counters the emergence of resistance mutations. In addition, and counterintuitively, they wanted "stealth" drugs that would not slow bacterial proliferation, which would confer a growth advantage to any bacterial mutants that resist the mutation-slowing drug itself. That is, drugs that are not antibiotics themselves. "We found that DEQ fulfilled both requirements. Given together with cipro, DEQ reduced the development of mutations that confer antibiotic resistance, both in laboratory cultures and in animal models of infection, and bacteria did not develop resistance to DEQ," said first author Yin Zhai, a postdoctoral associate in the Rosenberg lab. "In addition, we achieved this mutation-slowing effect at low DEQ concentrations, which is promising for patients. Future clinical trials are needed to evaluate the ability of DEQ to decelerate bacterial antibiotic resistance in patients." Other contributors to this work include John P. Pribis, Sean W. Dooling, Libertad Garcia-Villada, P.J. Minnick, Jun Xia, Jingjing Liu, Qian Mei, Devon M. Fitzgerald, Christophe Herman, P.J. Hastings and Mauro Costa-Mattioli. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine, the Dan L Duncan Comprehensive Cancer Center and Rice University. This work was supported by NIH Directors Pioneer Awards DP1-AI52073 and DP1-AG072751, and NIH grants R35-GM122598 and R01-CA250905, P30-AI036211, P30-CA125123 and S10-RR024574, the Dan L Duncan Comprehensive Cancer Center and the John S. Dunn Gulf Coast Consortium for Chemical Genomics. Further support was provided by the State of Nebraska LB595 and LB692 and NIH/NIEHS R00ES033259 awards.