预约演示
更新于：2025-05-23
Manidipine Hydrochloride
盐酸马尼地平
更新于：2025-05-23
概要
基本信息
原研机构- |
非在研机构- |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 意大利 (2000-06-09), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C35H39ClN4O6 |
InChIKeyUFIXGLLGFBWKAV-UHFFFAOYSA-N |
CAS号89226-75-5 |
关联
4
项与 盐酸马尼地平 相关的临床试验CTR20200873
盐酸马尼地平片在中国健康受试者空腹和餐后状态下单中心、随机、开放、双周期、双交叉设计的生物等效性试验
NCT03106597
Manidipine Versus Amlodipine in Patients With Hypertension: Effects on Peripheral Edema Evaluated by Bioimpedance Analysis
NCT00627952
Double Blind, Randomized, Parallel Group, Multicentre Study to Evaluate the Effects of Manidipine 20 MG Vs. Amlodipine 10 MG and the Combination of Manidipine 10 MG Plus Delapril 30 MG Vs. Amlodipine 5 MG Plus Delapril 30 MG on Intraglomerular Pressure in Hypertensive Patients
100 项与 盐酸马尼地平 相关的临床结果
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100 项与 盐酸马尼地平 相关的转化医学
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100 项与 盐酸马尼地平 相关的专利（医药）
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567
项与 盐酸马尼地平 相关的文献（医药）2025-05-01INTERNATIONAL IMMUNOPHARMACOLOGY
Regulation of P-glycoprotein through CaMKII/cPLA2 pathway in lymphocytes for treating refractory rheumatoid arthritis by manidipine
Article
作者: Li, Qi-Lu ; Huan, Qiu-Chan ; Qiu, Xuan-Tong ; Qu, Biao ; Yan, Yan-Hua ; Xie, Ying ; Zhou, Hua ; Qu, Yue
BACKGROUND:
Overexpression of P-glycoprotein (P-gp) in the lymphocytes were observed with patients with refractory rheumatoid arthritis (RRA) in previous clinical studies, which correlated with the resistance to multiple disease-modifying antirheumatic drugs (DMARDs). The underlying mechanisms is unknown, which leading to unmet therapeutic approach for RRA.
METHODS:
A modified adjuvant-induced arthritis (AA) rat model with overexpression of P-gp in lymphocytes and resistance to methotrexate (MTX) treatment at the reported anti-arthritis dosage was previous build and used for examining the anti-arthritic effects of MA in combination with MTX. Moreover, knock-down of CaMKII were used on P-gp overexpression THP-1 cell lines to understanding the underlying mechanisms of MA.
RESULTS:
MTX alone did not show anti-arthritis effects on AA model, while treatment of MA overcome the resistance to MTX by reducing the enhanced P-gp expression and enhancing the anti-arthritic effects of MTX in the AA rat model. Moreover, MA overcame the MTX resistance and improved the anti-inflammatory effect of MTX in P-gp-THP-1 cells as well as the lymphocytes isolated from AA rats. Mechanistically, our data indicated that MA reduced the P-gp expression through the CaMKII/cPLA2 pathway, leading to increased accumulation of rhodamine 123 and FITC-MTX.
CONCLUSION:
The elevated levels of CaMKII and cPLA2 contribute to the increased levels of P-gp (ABCB1) in lymphocytes of RRA with an inadequate response to MTX, revealing a novel mechanism of resistance. For the first time, our study indicated that MA maybe a promising treatment to overcome the MTX resistance in patients with active RRA.
2025-04-01CELL DEATH AND DIFFERENTIATION
UGT8 mediated sulfatide synthesis modulates BAX localization and dictates apoptosis sensitivity of colorectal cancer
Article
作者: Picavet-Havik, Daisy I ; Zhang, Le ; Zijlmans, Dick W ; Zijlmans, Dick W. ; Vaz, Frédéric M ; van der Wel, Nicole N. ; Atencia Taboada, Lidia ; Vaz, Frédéric M. ; Medema, Jan Paul ; Picavet-Havik, Daisy I. ; Ramesh, Prashanthi ; Vermeulen, Michiel ; van der Wel, Nicole N ; Roessler, Rebecca
Abstract:
Elevated de novo lipid synthesis is a remarkable adaptation of cancer cells that can be exploited for therapy. However, the role of altered lipid metabolism in the regulation of apoptosis is still poorly understood. Using thermal proteome profiling, we identified Manidipine-2HCl, targeting UGT8, a key enzyme in the synthesis of sulfatides. In agreement, lipidomic analysis indicated that sulfatides are strongly reduced in colorectal cancer cells upon treatment with Manidipine-2HCl. Intriguingly, this reduction led to severe mitochondrial swelling and a strong synergism with BH3 mimetics targeting BCL-XL, leading to the activation of mitochondria-dependent apoptosis. Mechanistically, Manidipine-2HCl enhanced mitochondrial BAX localization in a sulfatide-dependent fashion, facilitating its activation by BH3 mimetics. In conclusion, our data indicates that UGT8 mediated synthesis of sulfatides controls mitochondrial homeostasis and BAX localization, dictating apoptosis sensitivity of colorectal cancer cells.
2025-03-01CURRENT DRUG METABOLISM
Pharmacokinetic Interactions of Paxlovid Involving CYP3A Enzymes and P-gp Transporter: An Overview of Clinical Data
Review
作者: Kandasamy, Krishnaveni ; Maideen, Naina Mohamed Pakkir ; Balasubramanian, Rajkapoor
Background::
The US FDA has approved paxlovid, a combination of nirmatrelvir and ritonavir, as
the first oral treatment for the management of mild-to-moderate COVID-19 patients.
Objective::
The purpose of this review article is to explore the clinical data that is currently available regarding
the drug-drug interactions (DDIs) of paxlovid with various medications.
Methods::
Keywords, such as drug interactions, paxlovid, ritonavir, nirmatrelvir, pharmacokinetic interactions,
CYP3A, and P-glycoprotein, were used to search online databases, including LitCOVID, Scopus, Embase, EBSCO
host, Google Scholar, ScienceDirect, Cochrane Library, and reference lists.
Results::
Paxlovid interacted with a variety of medications due to strong inhibition of CYP3A4 and P-gp transporter
protein by ritonavir and the dual function of nirmatrelvir as a substrate and inhibitor of CYP3A enzymes
and P-gp transporter protein. Numerous case reports and other studies determined that the risk of toxicities
of several drugs, including anticoagulants (warfarin, rivaroxaban), calcium channel blockers (nifedipine,
manidipine, verapamil), statins (atorvastatin), immunosuppressants (tacrolimus), antiarrhythmics (amiodarone),
antipsychotics (clozapine, quetiapine), and ranolazine have been enhanced by the concomitant administration
of paxlovid.
Conclusion::
Adverse effects of paxlovid from DDIs can range from less-than-ideal therapeutic responses to
potentially fatal toxicities. Effective management requires close observation, adjustments to dosage, and assessment
of substitute treatments. Collaboration between pharmacists and other medical professionals is necessary
to guarantee effective and safe treatment outcomes of paxlovid therapy.
100 项与 盐酸马尼地平 相关的药物交易
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研发状态
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 原发性高血压 | 法国 | 2001-11-05 | |
| 原发性高血压 | 希腊 | 2001-11-05 | |
| 原发性高血压 | 意大利 | 2001-11-05 | |
| 原发性高血压 | 西班牙 | 2001-11-05 | |
| 高血压 | 意大利 | 2000-06-09 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
N/A | 53 | Manidipine/delapril 30/10mg | 構遞鑰觸蓋衊醖鑰築鹽(膚鹹鹹鹽淵衊鏇膚簾觸) = 範糧積繭獵艱醖築壓淵 鬱鹹糧簾艱觸衊艱壓觸 (夢壓鏇鹹鹽簾憲壓憲齋 ) 更多 | - | 2022-04-07 | ||
N/A | - | 283 | 醖艱積鏇窪膚廠築壓糧(艱選齋簾鏇積顧繭餘獵) = 獵鑰選顧鹽鹹鏇憲憲鹹 餘夢夢襯餘齋獵蓋構壓 (鑰糧願鬱壓餘壓獵餘壓 ) 更多 | 积极 | 2021-04-01 | ||
N/A | - | 糧簾築壓築簾襯構觸鬱(積願鏇鑰淵觸築淵壓窪) = 願夢構獵窪簾繭選淵願 餘觸網壓廠範鏇齋築積 (築遞醖醖構鹹鹽觸簾鏇, 3.9) 更多 | 积极 | 2010-06-01 | |||
糧簾築壓築簾襯構觸鬱(積願鏇鑰淵觸築淵壓窪) = 鹹蓋鏇齋襯窪獵觸衊艱 餘觸網壓廠範鏇齋築積 (築遞醖醖構鹹鹽觸簾鏇, 4.0) 更多 |
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