2. Metabolic Enzyme/Protease MAPK/ERK Pathway PI3K/Akt/mTOR NF-κB Immunology/Inflammation
  3. Phospholipase NADPH Oxidase p38 MAPK Akt NF-κB AP-1 Reactive Oxygen Species (ROS)
  4. MJ33

MJ-33 is a competitive phospholipase A₂ (PLA₂) inhibitor with an IC50 of 0.3 μM. MJ-33 inhibits the activation of NOX2 by blocking the PLA₂ activity of Prdx6, thereby reducing the production of ROS. MJ-33 effectively inhibits the activity of acidic PLA₂ (pH 4.0), reduces the degradation of pulmonary surfactant phosphatidylcholine (PC), but has no effect on alkaline PLA₂ (pH 8.5). MJ-33 significantly alleviates lung oxidative damage induced by ischemia-reperfusion (I/R). MJ-33 significantly inhibits the invasive, migratory and adhesive abilities of prostate cancer cells by suppressing the MAPK, AKT, NF-κB and AP-1 signaling pathways. MJ-33 can be used to study ROS-related diseases and prostate cancer.

For research use only. We do not sell to patients.

MJ33

MJ33 Chemical Structure

CAS No. : 137300-78-8

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MJ33 Related Antibodies

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Phospholipase A PLD Phospholipase C

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NOX1 NOX2 NOX4 NOX5 DUOX1

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

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Akt Akt1 Akt2 Akt3

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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c-Fos FosB Fra1/FOSL1 Fra2/FOSL2 c-Jun

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Description

MJ-33 is a competitive phospholipase A₂ (PLA₂) inhibitor with an IC50 of 0.3 μM. MJ-33 inhibits the activation of NOX2 by blocking the PLA₂ activity of Prdx6, thereby reducing the production of ROS. MJ-33 effectively inhibits the activity of acidic PLA₂ (pH 4.0), reduces the degradation of pulmonary surfactant phosphatidylcholine (PC), but has no effect on alkaline PLA₂ (pH 8.5). MJ-33 significantly alleviates lung oxidative damage induced by ischemia-reperfusion (I/R). MJ-33 significantly inhibits the invasive, migratory and adhesive abilities of prostate cancer cells by suppressing the MAPK, AKT, NF-κB and AP-1 signaling pathways. MJ-33 can be used to study ROS-related diseases and prostate cancer[1][2][3].

In Vitro

MJ33 (50-1000 nM; 24-48 h) 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) 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) 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) 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) 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) 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) 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) restores the GSH/ROS balance in cultured C57BL/6J primary hippocampal neurons with AAV-mediated D2HGDH knockdown, without affecting cell viability[2].
MJ33 completely inhibits NOX2-dependent ROS production in wild-type mPMVEC stimulated by AngII[3].
MJ33 (4 μM; 15 min) 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) 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 Related Antibodies

Cell Invasion Assay[1]

Cell Line: DU145 human prostate cancer cells
Concentration: 50, 100 and 200 nM
Incubation Time: 24 h
Result: Significantly inhibited DU145 cell invasion in a concentration-dependent manner, with inhibition ratios ranging from 15-70%.
Caused no cytotoxicity at tested concentrations after 24 h.

Cell Migration Assay [1]

Cell Line: DU145 human prostate cancer cells
Concentration: 50, 100 and 200 nM
Incubation Time: 24 h
Result: Significantly inhibited DU145 cell migration in a concentration-dependent manner, with inhibition ratios ranging from 30-75%.
Caused no cytotoxicity at tested concentrations after 24 h.

Western Blot Analysis[1]

Cell Line: DU145 human prostate cancer cells
Concentration: 50, 100 and 200 nM (6 h incubation for p-JNK, p-ERK, p-p38, p-AKT, NF-κB p65, c-fos, c-Jun); 50-200 nM (24 h incubation for MMP-2, MMP-9, u-PA)
Incubation Time: 6 h (p-JNK, p-ERK, p-p38, p-AKT, NF-κB p65, c-fos, c-Jun); 24 h (MMP-2, MMP-9, u-PA)
Result: Reduced protein levels of MMP-2, MMP-9, and u-PA in a concentration-dependent manner after 24 h treatment.
Reduced protein levels of phosphorylated JNK, ERK, p38, and AKT, as well as nuclear NF-κB p65, c-fos, and c-Jun, all in a concentration-dependent manner after 6 h treatment.
Left total JNK, ERK, p38, and AKT protein levels unchanged.
In Vivo

MJ33 (500 nmol/kg; intraperitoneal injection; once daily for 7 consecutive days) 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) 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) 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.

Animal Model: C57BL/6J (male, 28 days old, ~22-24 g at study start, hippocampal AAV-mediated D2HGDH knockdown, KA-induced epilepsy)[2]
Dosage: 500 nmol/kg
Administration: i.p.; daily; 7 days
Result: Reduced the number of spontaneous recurrent seizures per day.
Decreased the number of epileptic events detected via local field potentials.
Shortened the duration of single epileptic events.
Significantly reduced integrated DHE fluorescence density (a measure of ROS levels) in the hippocampal CA1, CA3, and DG regions.
Animal Model: C57BL/6 wild-type (10-week-old; male and female)[3]
Dosage: 0.4 nmol; 4 nmol; 10 nmol
Administration: intratracheal; intravenous
Result: Inhibited lung Prdx6 PLA2 activity by approximately 85% (reduced to ~15% of control levels) at 4 hours post-administration via both routes.
Showed only slight recovery of PLA2 activity at 24 hours, partial recovery at 48 hours, and returned to near control levels by 72 hours for 4 nmol and 10 nmol doses.
Achieved lung uptake of 67-87% of the injected dose for i.t.
delivery and 23-42% for i.v.
delivery at 4 hours post-administration.
Became undetectable in lungs at 72 hours post-administration via either route.
Animal Model: C57BL/6 wild-type (10-week-old)[3]
Dosage: 4 nmol
Administration: intravenous
Result: Reduced reperfusion-induced ROS production by 66% compared to untreated I/R lungs.
Reduced TBARS levels from 136 nmol/mg protein (untreated I/R) to 95.5 nmol/mg protein.
Reduced 8-isoprostane levels from 440 nmol/mg protein to 310 nmol/mg protein.
Reduced protein carbonyl levels from 9.25 nmol/mg protein to 7.00 nmol/mg protein.
Reduced lung wet/dry weight ratio from 7.35 to 6.35.
Molecular Weight

492.55

Formula

C22H44F3O6P
CAS No.
SMILES

O=P(OC)(O)OC(COCCCCCCCCCCCCCCCC)COCC(F)(F)F
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Room temperature in continental US; may vary elsewhere.
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MJ33 Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

MJ33137300-78-8MJ 33MJ-33PhospholipaseNADPH Oxidasep38 MAPKAktNF-κBAP-1Reactive Oxygen Species (ROS)NOXPKBProtein kinase BNuclear factor-κBNuclear factor-kappaBActivator Protein 1phospholipase A2 inhibitorNADPH oxidase (NOX2)reactive oxygen species (ROS)peroxiredoxin 6 (Prdx6)lung ischemia-reperfusion injuryantioxidant therapymetastatic inhibitionInhibitorinhibitorinhibit

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