Trimyristin [555-45-3]

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Cat# HY-N2511-100mg

Size : 100mg

Brand : MedChemExpress

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Description

Trimyristin is an orally active compound. Trimyristin can be isolated from the seeds of nutmeg (Myristica fragrans). Trimyristin inhibits the activities of acetylcholinesterase (AChE), ACP and ALP, with IC50 values of 0.11, 0.16 and 0.18 mM, respectively. Trimyristin exerts competitive-noncompetitive inhibition on acetylcholinesterase, uncompetitive inhibition on ACP, and competitive/noncompetitive inhibition on ALP. Trimyristin restores the downregulated acetylcholinesterase concentration in the cerebral cortex of rats exposed to sodium arsenite. Trimyristin can be used in studies related to fascioliasis and neurotoxicity[1][2].

IC50 & Target[1]

AChE

0.11 mM (IC50)

ACP

0.16 mM (IC50)

ALP

0.18 mM (IC50)

In Vitro

Trimyristin (0.04-0.15 mM; 15 min preincubation) potently inhibits AChE (IC50 = 0.11 mM), ACP (IC50 = 0.16 mM), and ALP (IC50 = 0.18 mM) in nervous tissue homogenates of Lymnaea acuminata snails via competitive noncompetitive inhibition of AChE and ALP, and uncompetitive inhibition of ACP[1].

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

In Vivo

Trimyristin (2.80-12.43 mg/L; aquatic exposure; 24 or 96 hours) causes significant, concentration- and time-dependent inhibition of AChE, ACP, and ALP in the nervous tissue of Lymnaea acuminata, with maximum inhibition of 37% for AChE, 36% for ACP, and 39% for ALP observed at the 80% 96 h LC50 dose[1].
Trimyristin (15-30 mg/kg; p.o.; daily; 6 weeks) restores sodium arsenite-induced downregulated cerebral cortex acetylcholinesterase concentrations to baseline control levels in adult male Wistar rats[2].
Trimyristin (15-30 mg/kg; p.o.; daily; 9 weeks) shows that chronic treatment with 30 mg/kg significantly reduces cerebral cortex acetylcholinesterase concentrations in adult male Wistar rats, while 15 mg/kg maintains control-level concentrations[2].

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

Animal Model: Lymnaea acuminata Lamarck (adults, length 2.25 cm)[1]
Dosage: 6.21 mg/L (40% of 24 h LC50); 12.43 mg/L (80% of 24 h LC50); 2.80 mg/L (40% of 96 h LC50); 5.60 mg/L (80% of 96 h LC50)
Administration: aquatic exposure; 24 or 96 hours
Result: Reduced acetylcholinesterase (AChE) activity to 90%, 82%, 73%, and 63% of control levels after exposure to 40% 24 h LC50, 80% 24 h LC50, 40% 96 h LC50, and 80% 96 h LC50 of trimyristin, respectively.
Reduced acid phosphatase (ACP) activity to 87%, 80%, 73%, and 64% of control levels after exposure to 40% 24 h LC50, 80% 24 h LC50, 40% 96 h LC50, and 80% 96 h LC50 of trimyristin, respectively.
Reduced alkaline phosphatase (ALP) activity to 92%, 84%, 71%, and 61% of control levels after exposure to 40% 24 h LC50, 80% 24 h LC50, 40% 96 h LC50, and 80% 96 h LC50 of trimyristin, respectively.
Caused statistically significant (P < .05) concentration- and time-dependent inhibition of AChE, ACP, and ALP, with maximum inhibition of 37% for AChE, 36% for ACP, and 39% for ALP observed at the 80% 96 h LC50 dose.
Animal Model: Wistar (adult male, 150-250 g, average 200 g, sodium arsenite-induced neurotoxicity)[2]
Dosage: 15 mg/kg; 30 mg/kg
Administration: p.o.; daily; 6 weeks
Result: Significantly upregulated and restored cerebral cortex AChE concentrations to baseline control levels.
Restored normal cytoarchitecture of cerebral cortices, with no significant inflammation or degenerative changes.
Animal Model: Wistar (adult male, 150-250 g, average 200 g)[2]
Dosage: 15 mg/kg; 30 mg/kg
Administration: p.o.; daily; 9 weeks
Result: Maintained AChE concentrations at levels comparable to control groups (15 mg/kg).
Caused a statistically significant reduction in cerebral cortex AChE concentrations relative to control groups (30 mg/kg).
Molecular Weight

723.16

Formula

C45H86O6

CAS No.
Appearance

Solid

Color

White to off-white

SMILES

CCCCCCCCCCCCCC(OC(COC(CCCCCCCCCCCCC)=O)COC(CCCCCCCCCCCCC)=O)=O

Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, sealed storage, away from moisture

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

Solvent & Solubility
In Vitro: 

Acetone : 5 mg/mL (6.91 mM; Need ultrasonic)

DMF : 2.5 mg/mL (3.46 mM; Need ultrasonic)

DMSO : < 1 mg/mL (insoluble or slightly soluble)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.3828 mL 6.9141 mL 13.8282 mL
5 mM 0.2766 mL 1.3828 mL 2.7656 mL
View the Complete Stock Solution Preparation Table

* 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.

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Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

In Vivo Dissolution Calculator
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Purity & Documentation
References