3062-14-4

Basic information

• Product Name: H-ASP-LEU-OH
• Synonyms: H-ASP-LEU-OH;L-ASPARTIC ACID-L-LEUCINE;Asp-Leu-OH;L-Asp-L-Leu-OH;N-L-α-Aspartyl-L-leucine;-aspartyl-L-leucine;N-L-&alpha
• CAS NO: 3062-14-4
• Molecular Formula: C10H18N2O5
• Molecular Weight: 246.26
• Mol File: 3062-14-4.mol
• Article Data: 3

Chemical Properties

• Boiling Point: 527.6°Cat760mmHg
• Flash Point: 272.9°C
• Appearance: /
• Density: 1.272g/cm³
• Vapor Pressure: 1.53E-12mmHg at 25°C
• Refractive Index: 1.516
• Storage Temp.: -15°C
• Solubility: Chloroform (Very Slightly, Heated, Sonicated), Water (Slightly)
• PKA: 2.99±0.10(Predicted)
• Stability: Hygroscopic
• CAS DataBase Reference: H-ASP-LEU-OH(CAS DataBase Reference)
• NIST Chemistry Reference: H-ASP-LEU-OH(3062-14-4)
• EPA Substance Registry System: H-ASP-LEU-OH(3062-14-4)

Safety Data

• Hazardous Substances Data: 3062-14-4(Hazardous Substances Data)

Usage

General Description

H-ASP-LEU-OH is a chemical compound consisting of the amino acids aspartic acid and leucine, connected by peptide bonds. Aspartic acid is a non-essential amino acid that plays a key role in the citric acid cycle and in the production of other amino acids. Leucine is an essential amino acid that is important for protein synthesis and muscle growth. When combined in the form of H-ASP-LEU-OH, these two amino acids may have potential applications in the fields of biochemistry, medicinal chemistry, and pharmaceuticals, as they can be used in the development of new drugs and therapies. However, further research is needed to fully understand the properties and potential uses of this compound.

InChI:InChI=1/C10H18N2O5/c1-5(2)3-7(10(16)17)12-9(15)6(11)4-8(13)14/h5-7H,3-4,11H2,1-2H3,(H,12,15)(H,13,14)(H,16,17)

Upstream product

• 119278-21-6 N-(O-benzyl-N-benzyloxycarbonyl-L-α-aspartyl)-L-leucine benzyl ester 
• 1738-69-8 L-Leucine benzyl ester 
• 2462-35-3 L-leucine benzyl ester hydrochloride 

Relevant articles and documents

DPP4 INHIBITOR AND PHARMACEUTICAL APPLICATION THEREOF

The present invention provides a Dpp4 inhibitor which comprises a leucine derivative of the following formula (1) or a methionine derivative of the following formula (2): wherein each R1 and R3 represents a hydrogen atom (H) and an L-amino acid residue; R2 represents a hydroxyl group (OH), alkoxy group having 1 to 6 carbon atoms, amino group (NH2), alkylamino group having 1 to 6 carbon atoms, glycine residue, β-alanine residue, L-amino acid (except for proline, alanine and phenylalanine) residue or L-amino-acid amide (except for proline amide, alanine amide and phenylalanine amide) residue; and R4 represents a hydroxyl group (OH), alkoxy group having 1 to 6 carbon atoms, amino group (NH2), alkylamino group having 1 to 6 carbon atoms, glycine residue, β-alanine residue, L-amino acid (except for proline and alanine) residue or L-amino-acid amide (except for proline amide and alanine amide) residue. These derivatives also act as autophagy regulators.

Isolation and identification of urinary β-aspartyl dipeptides and their concentrations in human urine

β-Aspartyl-methionine, -aspartic acid and -glutamic acid and γ-glutamyl-threonine and -glycine were isolated and identified in human urine by means of ion-exchange chromatography, highvoltage paper electrophoresis, acid hydrolysis and determination of N-terminal amino acids of the isolated compounds, and comparison of their behaviors in paper electrophoresis and chromatography with those of the authentic compounds. The concentrations of acidic β-aspartyl dipeptides in human urine were determined using an amino acid analyzer. Their concentrations were as follows: β-aspartyl-glycine, male, 44.4±8.5, female, 61.4±18.9, child, 83.7±27.1; -alanine, male, 11.0±4.9, female, 20.7±12.0, child, 25.3±9.1; -glutamic acid, male, 10.0±3.7, female, 23.0±8.5, child, 20.4±7.5; -serine, male, 9.9±2.8, female, 13.6±3.8, child, 14.9±4.7; -aspartic acid, male, 4.3±1.0, female, 9.1±2.2, child, 18.4±6.5; -threonine, male, 3.9±0.9, female, 5.8±1.1, child, 13.2±4.9 μmol/g creatinine (mean ± S.D.). The order of the sum of their concentrations tended to be child>female>male. Patients receiving intravenous hyperalimentation also excreted acidic β-aspartyl dipeptides into urine in amounts similar to those in females and in a pattern similar to that observed in healthy persons. This finding indicates that urinary β-aspartyl dipeptides were probably of endogenous origin because oral nutrition was stringently excluded in these patients.