Mefloquine Hydrochloride - CAS 51773-92-3
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Not Intended for Therapeutic Use. For research use only.
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Mefloquine HCl is a blood schizonticide by inhibiting hemozoin formation, used as an antimalarial drug.
Publictions citing BOC Sciences Products
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1.Adverse neuropsychiatric effects of antimalarial drugs.
Grabias B1, Kumar S1. Expert Opin Drug Saf. 2016 Apr 14. [Epub ahead of print]
Antimalarial drugs are the primary weapon to treat parasite infection, save lives, and curtail further transmission. Accumulating data have indicated that at least some antimalarial drugs may contribute to severe neurological and/or psychiatric side effects which further complicates their use and limits the pool of available medications. Areas Covered: In this review article, we summarize published scientific studies in search of evidence of the neuropsychiatric effects that may be attributed to the commonly used antimalarial drugs administered alone or in combination. Each individual drug was used as a search term in addition to keywords such as neuropsychiatric, adverse events, and neurotoxicity. Expert Opinion: Accumulating data based on published reports over several decades have suggested that among the major commonly used antimalarial drugs, only mefloquine exhibited clear indications of serious neurological and/or psychiatric side effects.
2.Pannexin-1 channels do not regulate α1-adrenoceptor-mediated vasoconstriction in resistance arteries.
Angus JA1, Betrie AH2, Wright CE3. Eur J Pharmacol. 2015 Mar 5;750:43-51. doi: 10.1016/j.ejphar.2015.01.024. Epub 2015 Jan 28.
Recent reports have provided evidence for a new concept that in small resistance arteries α1D-adrenoceptor-mediated contraction is intimately linked to pannexin-1 (Px1) hemichannels that open to allow the release of ATP, from the smooth muscle effector cell, that acts back on P2Y purinoceptors to cause contraction. This concept mainly relied on using mefloquine 10-20μM as a putative selective Px1 channel-blocking agent to completely inhibit the contraction to phenylephrine, but not K(+) 40mM. Lower concentrations of mefloquine had no effect. The purpose of the present study was to explore the specificity of mefloquine for Px1 channels and the role of these channels in small artery contraction. In mouse and rat isolated small resistance arteries, either pressurised or set up for wire myography, the effects of mefloquine on contractions to K(+), phenylephrine and a range of vasoconstrictor agents were assessed and compared with the Px1 channel inhibitor carbenoxolone.
3.CRISPR-Cas9-modified pfmdr1 protects Plasmodium falciparum asexual blood stages and gametocytes against a class of piperazine-containing compounds but potentiates artemisinin-based combination therapy partner drugs.
Ng CL1, Siciliano G2, Lee MC1, de Almeida MJ, Corey VC3, Bopp SE3, Bertuccini L4, Wittlin S5, Kasdin RG1, Le Bihan A6, Clozel M6, Winzeler EA3, Alano P2, Fidock DA1,7. Mol Microbiol. 2016 Apr 12. doi: 10.1111/mmi.13397. [Epub ahead of print]
Emerging resistance to first-line antimalarial combination therapies threatens malaria treatment and the global elimination campaign. Improved therapeutic strategies are required to protect existing drugs and enhance treatment efficacy. We report that the piperazine-containing compound ACT-451840 exhibits single-digit nanomolar inhibition of the Plasmodium falciparum asexual blood stages and transmissible gametocyte forms. Genome sequence analyses of in vitro-derived ACT-451840-resistant parasites revealed single nucleotide polymorphisms in pfmdr1, which encodes a digestive vacuole membrane-bound ABC transporter known to alter P. falciparum susceptibility to multiple first-line antimalarials. CRISPR-Cas9 based gene editing confirmed that PfMDR1 point mutations mediated ACT-451840 resistance. Resistant parasites demonstrated increased susceptibility to the clinical drugs lumefantrine, mefloquine, quinine, and amodiaquine. Stage V gametocytes harboring Cas9-introduced pfmdr1 mutations also acquired ACT-451840 resistance.
4.Anti-malarial Drugs Primaquine and Chloroquine Have Different Sensitization Effects with Anti-mitotic Drugs in Resistant Cancer Cells.
Choi AR1, Kim JH1, Woo YH1, Kim HS2, Yoon S3. Anticancer Res. 2016 Apr;36(4):1641-8.
The purpose of this study was to identify conditions that would increase the sensitivity of drug-resistant cancer cells. Previously, two anti-malarial drugs, chloroquine (CHL) and primaquine (PRI), showed different sensitization effects for vinblastine (VIB)-resistant cancer cells. Herein, we tested co-treatment of cells with CHL or PRI and other microtubule-targeting cancer drugs, namely, vinorelbine (VIO), paclitaxel (PAC), docetaxel (DOC), vincristine (VIC), or halaven (HAL). We found that PRI sensitized P-glycoprotein (P-gp)-overexpressing drug-resistant KBV20C cells to all six anti-mitotic drugs to a similar extent. CHL had a similar sensitization effect only for co-treatment with PAC, DOC, VIC, and HAL, while the sensitization effect was less marked for co-treatment with VIB or VIO. FACS analysis and western blot analysis revealed that G2arrest and apoptosis showed only a slight increase on co-treatment with VIB or VIO and CHL. We also found that phospho-histone H3 and pRb were markedly increased only by PRI-VIB co-treatment, but not by CHL-VIB co-treatment.
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CAS 51773-92-3 Mefloquine Hydrochloride

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