1. Metabolic Enzyme/Protease
  2. Lipoxygenase
  3. ML351

ML351 

Cat. No.: HY-111310 Purity: 98.19%
Handling Instructions

ML351 is a potent and highly specific 15-LOX-1 inhibitor with an IC50 of 200 nM. ML351 shows excellent selectivity (>250-fold) versus the related isozymes, 5-LOX, platelet 12-LOX, 15-LOX-2, ovine COX-1, and human COX-2. ML351 prevents dysglycemia and reduces β-cell oxidative stress in nonobese diabetic mouse model of T1D.

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

ML351 Chemical Structure

ML351 Chemical Structure

CAS No. : 847163-28-4

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100 mg USD 1550 In-stock
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Description

ML351 is a potent and highly specific 15-LOX-1 inhibitor with an IC50 of 200 nM. ML351 shows excellent selectivity (>250-fold) versus the related isozymes, 5-LOX, platelet 12-LOX, 15-LOX-2, ovine COX-1, and human COX-2[1]. ML351 prevents dysglycemia and reduces β-cell oxidative stress in nonobese diabetic mouse model of T1D[2].

In Vitro

ML351 (1-50 μM; 24 hours) displays no deleterious effects on cellular apoptosis (by caspase activity assay)[2].
ML351 (10-50 μM; 24 h) protects mouse islets in a T1D model in vitro. Islets exposed to proinflammatory cytokines exhibits increased insulin release at 2.5 mM glucose and impaired insulin release in response to 25 mM glucose. However, ML351 restores insulin secretion at 2.5 mmol/L glucose to control levels, and insulin release in response to 25 mM glucose is significantly improved compared with treatment with proinflammatory cytokines alone[2].
ML351 reverses the stimulation of ROS production in mouse islets in response to proinflammatory cytokines in vitro[2].

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

In Vivo

ML351 (0-48 mg/kg; before the beginning of the STZ series and concluding 5 days after the last dose of STZ) protects against diabetes development in an STZ β-cell injury model. ML351 at 24 mg/kg (M24)+ STZ shows significantly less weight reduction compares with control group. M24 shows almost complete protection from hyperglycemia. But M48 and M0 exhibits frank hyperglycemia by day 9 of the study and significantly impaired GTTs[2].
ML351 (intraperitoneal injection; 0-24 mg/kg; daily for 2 weeks) leads to improved glycemic control and significantly reduced insulitis. The reduction of β-cell death in NOD mice has been suggested to lead to reductions in insulitis, likely by mitigating the chemotactic signals released by dying β-cells. NOD + M24 animals exhibited improved glycemic control compared with NOD + M0 animals[2].

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

Animal Model: Nine-week-old male C57BL/6J mice[2]
Dosage: 0 mg/kg; 24 mg/kg; 48 mg/kg;
Administration: Intraperitoneal injection before the beginning of the STZ series and concluding 5 days after the last dose of STZ
Result: Protected against diabetes development in an STZ β-cell injury model that mimics the inflammation seen in T1D.
Animal Model: Female NOD mice develop spontaneous autoimmune diabetes between 12 and 24 weeks of age[2]
Dosage: 0 mg/kg; 24 mg/kg; 48 mg/kg;
Administration: Intraperitoneal injection before the beginning of the STZ series and concluding 5 days after the last dose of STZ
Result: Protected Against Early Glycemic Deterioration in NOD Mice.
Molecular Weight

249.27

Formula

C₁₅H₁₁N₃O

CAS No.
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Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 125 mg/mL (501.46 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 4.0117 mL 20.0586 mL 40.1171 mL
5 mM 0.8023 mL 4.0117 mL 8.0234 mL
10 mM 0.4012 mL 2.0059 mL 4.0117 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.08 mg/mL (8.34 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
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ML351
Cat. No.:
HY-111310
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