MJ33 lithium salt 

MJ-33 lithium salt is a competitive phospholipase A₂ (PLA₂) inhibitor with an IC₅₀ of 0.3 μM. MJ-33 lithium salt inhibits NOX2 activation and reduces ROS production by blocking the PLA₂ activity of Prdx6. MJ-33 lithium salt effectively inhibits the activity of acidic PLA₂ (pH 4.0) and reduces the degradation of alveolar surfactant phosphatidylcholine (PC), but exerts no effect on alkaline PLA₂ (pH 8.5). MJ-33 lithium salt significantly alleviates lung oxidative injury induced by ischemia-reperfusion (I/R). MJ-33 lithium salt significantly inhibits the invasion, migration and adhesion abilities of prostate cancer cells by suppressing the MAPK, AKT, NF-κB and AP-1 signaling pathways. MJ-33 lithium salt can be used for the research of ROS-related diseases and prostate cancer^[1][2][3].

MJ33 (50-1000 nM; 24-48 h) lithium salt reduces the viability of DU145, LNCaP and PC-3 human prostate cancer cells in a concentration-dependent manner, with DU145 cells showing the highest sensitivity and an EC₅₀ of 458.32 nM after 24 h of incubation^[1].
MJ33 (50-200 nM; 24 h) lithium salt inhibits the invasion of human prostate cancer cell line DU145 in a concentration-dependent manner, with an inhibition rate of 15%-70% observed after treatment at 50-200 nM for 24 h, and this effect is independent of cytotoxicity^[1].
MJ33 (50-200 nM; 24 h) lithium salt inhibits the migration of human prostate cancer cell line DU145 in a concentration-dependent manner, with an inhibition rate of 30%-75% observed after treatment at 50-200 nM for 24 h, and this effect is independent of cytotoxicity^[1].
MJ33 (50-200 nM; 24 h) lithium salt inhibits the adhesion of DU145 human prostate cancer cells in a concentration-dependent manner, with an inhibition rate of 10%-45% observed after treatment at 50-200 nM for 24 h, and this effect is independent of cytotoxicity^[1].
MJ33 (50-200 nM; 24 h) lithium salt reduces the enzymatic activities of MMP-2, MMP-9 and u-PA in DU145 human prostate cancer cells in a concentration-dependent manner^[1].
MJ33 (50-200 nM; 6-24 h) lithium salt reduces the protein levels of MMP-2, MMP-9 and u-PA in a concentration-dependent manner in DU145 human prostate cancer cells after 24 h of incubation, and decreases the levels of phosphorylated JNK, ERK, p38, AKT as well as nuclear NF-κB p65, c-fos and c-Jun after 6 h of incubation^[1].
MJ33 (100-200 nM; 6 h) lithium salt inhibits the DNA-binding activities of NF-κB and AP-1 in DU145 human prostate cancer cells in a concentration-dependent manner^[1].
MJ33 (20 μM; 24 h) lithium salt restores the GSH/ROS balance in cultured C57BL/6J primary hippocampal neurons with AAV-mediated D2HGDH knockdown, without affecting cell viability^[2].
MJ33 lithium salt completely inhibits NOX2-dependent ROS production in wild-type mPMVEC stimulated by AngII^[3].
MJ33 (4 μM; 15 min) lithium salt reduces concanavalin A (Con A)-stimulated NOX2-dependent O₂^•− production by 79% in bone marrow neutrophils (PMNs) from wild-type mice^[3][4].
MJ33 (5-25 μM; 2-10 day) lithium salt exerts no effect on the proliferation or clonogenic survival of human lung cancer cell line A549 at concentrations up to 25 μM over an exposure period of up to 10 days^[3][4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

MJ33 (500 nmol/kg; intraperitoneal injection; once daily for 7 consecutive days) lithium salt reverses the increased epileptic susceptibility and elevated hippocampal ROS levels caused by D2HGDH knockdown in mouse epilepsy models^[2].
MJ33 (0.4-10 nmol; intratracheal administration; intravenous administration; single administration) lithium salt inhibits pulmonary Prdx6 PLA₂ activity in mice by approximately 85%, and the activity recovers in a dose-dependent manner within 72 h; among the administration routes, intratracheal administration results in higher pulmonary uptake, while intravenous administration leads to moderate pulmonary uptake^[3].
MJ33 (4 nmol; intravenous injection) lithium salt reduces ROS production by 66% in a mouse model of lung ischemia/reperfusion injury, and essentially abolishes oxidative stress and increased pulmonary permeability^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

498.48

C₂₂H₄₃F₃LiO₆P

1007476-63-2

Solid

White to off-white

O=P(OC)(OC(COCC(F)(F)F)COCCCCCCCCCCCCCCCC)O[Li]

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Hour MJ, et al. Antitumor effects of the novel quinazolinone MJ-33: inhibition of metastasis through the MAPK, AKT, NF-κB and AP-1 signaling pathways in DU145 human prostate cancer cells. Int J Oncol. 2012;41(4):1513-1519.  [Content Brief]

  [2]. Zhang Z, et al. D2HGDH Deficiency Regulates Seizures through GSH/Prdx6/ROS-Mediated Excitatory Synaptic Activity. Adv Sci (Weinh). 2025;12(13):e2404488.  [Content Brief]

  [3]. Lee I, et al. A novel nontoxic inhibitor of the activation of NADPH oxidase reduces reactive oxygen species production in mouse lung. J Pharmacol Exp Ther. 2013;345(2):284-296.  [Content Brief]