60254-83-3

Basic information

• Product Name: (DES-TYR1)-LEU-ENKEPHALIN
• Synonyms: des-tyr(1)-enkephalin-le;ENKEPHALIN (DES TYR2, LEU4);[DES-TYR1,LEU5]-ENKEPHALIN;(DES-TYR1)-LEU-ENKEPHALIN;GLY-GLY-PHE-LEU;H-GLY-GLY-PHE-LEU-OH;enkephalin-Leu, des-Tyr(1)-
• CAS NO: 60254-83-3
• Molecular Formula: C₁₉H₂₈N₄O₅
• Molecular Weight: 392.45
• Mol File: 60254-83-3.mol

Chemical Properties

• Boiling Point: 784.6°C at 760 mmHg
• Flash Point: 428.3°C
• Appearance: /
• Density: 1.222g/cm³
• Vapor Pressure: 6.3E-26mmHg at 25°C
• Refractive Index: 1.552
• Storage Temp.: -15°C
• PKA: 3.39±0.10(Predicted)
• CAS DataBase Reference: (DES-TYR1)-LEU-ENKEPHALIN(CAS DataBase Reference)
• NIST Chemistry Reference: (DES-TYR1)-LEU-ENKEPHALIN(60254-83-3)
• EPA Substance Registry System: (DES-TYR1)-LEU-ENKEPHALIN(60254-83-3)

Safety Data

• Hazardous Substances Data: 60254-83-3(Hazardous Substances Data)

Usage

Uses

Used in Pharmaceutical Industry:
(DES-TYR1)-LEU-ENKEPHALIN is used as an analgesic agent for its ability to produce pain-relieving effects by binding to opioid receptors in the brain and spinal cord. Its enhanced stability and blood-brain barrier penetration make it a more effective and longer-lasting alternative to traditional opioids for managing acute and chronic pain.
Used in Addiction Treatment:
In the field of addiction medicine, (DES-TYR1)-LEU-ENKEPHALIN is utilized as a therapeutic agent to help manage withdrawal symptoms and cravings associated with opioid dependence. Its agonist activity at opioid receptors can provide relief from the discomfort of withdrawal, potentially aiding in the recovery process for individuals struggling with addiction.
These applications highlight the versatility of (DES-TYR1)-LEU-ENKEPHALIN in both pain management and addiction treatment, underscoring its potential as a valuable asset in the pharmaceutical industry for addressing significant health challenges.

InChI:InChI=1/C19H28N4O5/c1-12(2)8-15(19(27)28)23-18(26)14(9-13-6-4-3-5-7-13)22-17(25)11-21-16(24)10-20/h3-7,12,14-15H,8-11,20H2,1-2H3,(H,21,24)(H,22,25)(H,23,26)(H,27,28)/t14-,15-/m0/s1

Upstream product

• 13171-93-2 N-benzyloxycarbonyl-L-glycyl-L-glycyl-L-phenylalanine 
• 15027-03-9 Z-Gly-Gly-L-Phe-OMe 
• 69983-47-7 N-Cbz-Gly-Gly-Phe-Leu-OH 
• 68835-85-8 N-benzyloxycarbonyl-glycyl-glycyl-(S)phenylalanyl-(S)leucine methyl ester 
• 129785-81-5 phospho-Tyr-Gly-Gly-Phe-Leu-OH 
• 4530-20-5 BOC-glycine 
• 81678-16-2 leucine enkephalin acetate 

Downstream Products

• 669775-05-7 H-Gly-Gly-L-Phe(4-I)-L-Leu-OH 
• 63-91-2 L-phenylalanine 

Relevant articles and documents

Rational Design of Small Peptides for Optimal Inhibition of Cyclooxygenase-2: Development of a Highly Effective Anti-Inflammatory Agent

Among the small peptides 2-31, (H)Gly-Gly-Phe-Leu(OMe) (30) reduced prostaglandin production of COX-2 with an IC50 of 60 nM relative to 6000 nM for COX-1. The 5 mg kg-1 dose of compound 30 rescued albino mice by 80% from capsaicin-induced paw licking and recovered it by 60% from carrageenan-induced inflammation. The mode of action of compound 30 for targeting COX-2, iNOS, and VGSC was investigated by using substance P, l-arginine, and veratrine, respectively, as biomarkers. The interactions of 30 with COX-2 were supported by isothermal calorimetry experiments showing a Ka of 6.10 ± 1.10 × 104 M-1 and ΔG of -100.3 kJ mol-1 in comparison to a Ka 0.41 × 103 ± 0.09 M-1 and ΔG of -19.2 ± 0.06 kJ mol-1 for COX-1. Moreover, compound 30 did not show toxicity up to a 2000 mg kg-1 dose. Hence, we suggest peptide 30 as a highly potent and promising candidate for further development into an anti-inflammatory drug.

Phosphorylation of enkephalins enhances their proteolytic stability

Pharmacological action of enkephalins as opioid peptides is limited because of their rapid degradation by endoproteases. A novel approach is used in this study to prolong the life of those peptides. Phosphorylation of N-terminal tyrosine residue is found to have a profound influence in improving the stability of [Met]enkephalin and [Leu]enkephalin against the action of aminopeptidase M. Whereas, breakdown of [Met]enkephalin and [Leu]enkephalin is essentially complete in less than one min when incubated at 37°C with purified aminopeptidase M (EC 3.4.11.2; substrate:enzyme = 1:0.1) in Tris buffer (pH 7.02), the corresponding phospho analogs are still detected 60 min after start of incubation. The rate of disappearance of phospho-[Met]enkephalin and phospho-[Leu]enkephalin follows first-order kinetics with half-lives of 7.3 and 8.8 min, respectively.

Transmucosal delivery of leucine enkephalin: Stabilization in rabbit enzyme extracts and enhancement of permeation through mucosae

Leucine enkephalin (Tyr-Gly-Gly-Phe-Leu; Leu-Enk) is a naturally occurring peptide that has been shown to have pain modulating properties. To evaluate the feasibility of using various absorptive mucosae as a route of systemic delivery, the stability of Leu-Enk and the effect of enzyme inhibitors (e.g., amastatin, EDTA, and thimerosal) on stabilization and permeation of Leu-Enk through rabbit mucosae in the presence of dihydrofusidates were investigated. Enzymes in the nasal, rectal, and vaginal mucosae were extracted and Leu-Enk (50 μg/mL) was added to each of the enzyme extracts and incubated to determine the kinetics and mechanism of degradation. The rate of degradation in the extracts in the absence of inhibitors followed the order: rectal > vaginal > nasal. Whereas EDTA had the best stabilizing effect on Leu-Enk, thimerosal was the best stabilizer for the degradation intermediates. A combination of amastatin (50 μM), EDTA (5 mM), and thimerosal (50 μM) had the greatest stabilizing effect on Leu-Enk and its degradation intermediates. For permeation studies, each mucosa was mounted onto a Valia-Chien permeation cell with Leu-Enk (200 μg/mL) in isotonic phosphate buffer (as donor solution). The enhancers used for the study were sodium tauro-dihydrofusidate (STDHF), sodium glycodihydrofusidate (SGDHF), and phosphato-dihydrofusidate (PHDHF). The greatest effect was achieved by PHDHF for all the mucosae. STDHF had a significant effect only on the rectal permeation, whereas SGDHF had significant effects on rectal and vaginal mucosae. Mechanisms by which the dihydrofusidates enhance permeation may involve micelle formation. Thus, the use of enzyme inhibitors and dihydrofusidates in combination has made transmucosal delivery of Leu-Enk a viable option.

" Mediator Methodology" for the Synthesis of Peptides in a Two-Polymeric System

Abstract: A novel methodology is described for a potential automated self-controlled synthesis of peptides.The method is based on transferring an N-protected amino acid from one insoluble polymer (donor) such as a polymeric o-nitrophenyl ester (a "bank" of active ester) to an insoluble polymer-bound amino acid (acceptor),with the aid of a soluble mediator molecule (shadchan)2 The method gives high yields of pure peptides by garanteeing stoichiomeric supply of the active ester and allowing self monitoring.When the polymer-bound (dimethylamino)pyridinium salts, the condensation reaction was expended to also include sulfonation and particularly phosphorylation reactions.