product name Mefloquine HCl
Description: Mefloquine HCl is a blood schizonticide by inhibiting hemozoin formation, it is used as an antimalarial drug. Mefloquine is widely used in both the treatment and prophylaxis of Plasmodium falciparum malaria. Mefloquine can induces oxidative stress in vitro. Evidence indicates that reactive oxygen species (ROS) may be used as a therapeutic modality to kill cancer cell. Mefloquine inhibited KvLQT1/minK channel currents with an IC50 value of approximately 1 μM. Mefloquine slowed the activation rate of KvLQT1/minK and more block was evident at lower membrane potentials compared with higher ones.
References: J Pharmacol Exp Ther. 2001 Oct;299(1):290-6; Oncol Lett. 2013 May;5(5):1541-1545.
414.77
Formula
C17H17ClF6N2O
CAS No.
51773-92-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 82 mg/mL (197.7 mM)
Water: <1 mg/mL
Ethanol: 82 mg/mL (197.7 mM)
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: Mefloquine is a quinoline antimalarial drug that is structurally related to the antiarrhythmic agent quinidine. Mefloquine is widely used in both the treatment and prophylaxis of Plasmodium falciparum malaria. MQ can induces oxidative stress in vitro. Evidence indicates that reactive oxygen species (ROS) may be used as a therapeutic modality to kill cancer cells. Kinase Assay: Cell Assay: Mefloquine inhibitedKvLQT1/minK channel currents with an IC50 value of approximately 1 microM. Mefloquine slowed the activation rate of KvLQT1/minK and more block was evident at lower membrane potentials compared with higher ones. HERG channel currents were about 6-fold less sensitive to block by mefloquine (IC50 = 5.6 microM). Block of HERG displayed a positive voltage dependence with maximal inhibition obtained at more depolarized potentials. MQ has a highly selective cytotoxicity that inhibits PCa cell growth. MQ-mediated ROS simultaneously downregulated Akt phosphorylation and activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and adenosine monophosphate-activated protein kinase (AMPK) signaling in PC3 cells. |
|---|---|
| In Vivo | Pregnant rats were treated orally with AS (15 and 40 mg/kg body weight (bwt)/day), MQ (30 and 80 mg/kg bwt/day) and AS/MQ (15/30 and 40/80 mg/kg bwt/day) on days 9-11 post coitum (pc). The dams were euthanized on day 12 pc and gestational and embryos histological parameters were evaluated. |
| Animal model | 30 and 80 mg/kg; oral gavage |
| Formulation & Dosage | |
| References | J Pharmacol Exp Ther. 2001 Oct;299(1):290-6; Oncol Lett. 2013 May;5(5):1541-1545; Hum Exp Toxicol. 2013 Sep;32(9):930-41. |
