D-Leucine amide hydrochloride
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D-Leucine amide hydrochloride

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Category
D-Amino Acids
Catalog number
BAT-003528
CAS number
80970-09-8
Molecular Formula
C6H14N2O·HCl
Molecular Weight
166.70
D-Leucine amide hydrochloride
IUPAC Name
(2R)-2-amino-4-methylpentanamide;hydrochloride
Synonyms
D-Leu-NH2 HCl; (R)-2-Amino-4-methylpentanamide hydrochloride
Appearance
White to off-white powder
Purity
≥ 98% (HPLC)
Density
0.98g/cm3
Melting Point
213-220 °C
Storage
Store at 2-8 °C
InChI
InChI=1S/C6H14N2O.ClH/c1-4(2)3-5(7)6(8)9;/h4-5H,3,7H2,1-2H3,(H2,8,9);1H/t5-;/m1./s1
InChI Key
VSPSRRBIXFUMOU-NUBCRITNSA-N
Canonical SMILES
CC(C)CC(C(=O)N)N.Cl
1. Involvement of capsaicin-sensitive afferent nerves in the proteinase-activated receptor 2-mediated vasodilatation in the rat dura mater
M Dux, J Rosta, P Sántha, G Jancsó Neuroscience. 2009 Jul 7;161(3):887-94. doi: 10.1016/j.neuroscience.2009.04.010. Epub 2009 Apr 8.
Neurogenic inflammation of the dura mater encephali has been suggested to contribute to the mechanisms of meningeal nociception and blood flow regulation. Recent findings demonstrated that the rat dura mater is innervated by trigeminal capsaicin-sensitive peptidergic nociceptive afferent nerves which mediate meningeal vascular responses through activation of the transient receptor potential vanilloid type 1 (TRPV1) receptor. The present work explored the functional significance of the capsaicin-sensitive subpopulation of dural afferent nerves via their contribution to the meningeal vascular responses evoked through activation of the proteinase-activated receptor 2 (PAR-2). The vascular responses of the dura mater were studied by laser Doppler flowmetry in a rat open cranial window preparation. Topical applications of trypsin, a PAR-2-activator, or Ser-Leu-Ile-Gly-Arg-Leu-amide (SLIGRL-NH(2)), a selective PAR-2 agonist peptide, resulted in dose-dependent increases in meningeal blood flow. The SLIGRL-NH(2)-induced vasodilatation was significantly reduced following capsaicin-sensitive afferent nerve defunctionalization by prior systemic capsaicin treatment and by pretreatment of the dura mater with the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP(8-37). Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME) an unspecific inhibitor of nitric oxide (NO) production, but not 1-(2-trifluoromethylphenyl) imidazole (TRIM), a neuronal NO synthase inhibitor, also inhibited the vasodilator response to SLIGRL-NH(2). The vasodilator responses elicited by very low concentrations of capsaicin (10 nM) were significantly enhanced by prior application of SLIGRL-NH(2). The present findings demonstrate that activation of the PAR-2 localized on capsaicin-sensitive trigeminal nociceptive afferent nerves induces vasodilatation in the dural vascular bed by mechanisms involving NO and CGRP release. The results indicate that the PAR-2-mediated activation and sensitization of meningeal capsaicin-sensitive C-fiber nociceptors may be significantly implicated in the pathophysiology of headaches.
2. Effect of L-leucinamide hydrochloride on experimental inflammation
B R Madan, A Al-Motrefi Res Commun Chem Pathol Pharmacol. 1987 Dec;58(3):393-6.
L-leucinamide hydrochloride, an amino acid derivative, was found to share the ability of phenylbutazone in attenuating the phlogistic response induced by intraplantar injection of formaldehyde and nystatin in the unanesthetized rat. In the granuloma pouch induced by the injection of air and croton oil, chronic administration of the drug for 7 days resulted in significant reduction in the volume of exudate and the weight of granulation tissue. While the mechanism of anti-inflammatory action has not been elucidated, it seems that the pituitary-adrenal system is not involved since there was no change in the weight of the adrenals. Of interest is the finding that leucinamide, unlike phenylbutazone, failed to produce gastric ulcers in the effective anti-inflammatory doses.
3. Proteinase-activated receptor 2 blockade impairs CCL11- or allergen-induced eosinophil recruitment in experimental pleurisy
Natália A Matos, Josiane F Silva, Karine A Damasceno, Geovanni D Cassali, Virginia S Lemos, Igor D G Duarte, André Klein Eur J Pharmacol. 2014 Oct 5;740:627-33. doi: 10.1016/j.ejphar.2014.06.018. Epub 2014 Jun 24.
Although proteinase-activated receptor (PAR)-2 has been implicated in inflammatory diseases, its role in regulating eosinophil recruitment in response to chemoattractants remains unclear. Here, we investigated the role of PAR-2 and PAR-2-activating Mast Cell (MC) tryptase on chemokine C-C motif ligand (CCL)11- and antigen-induced eosinophil recruitment to the pleural cavity of BALB/c mice. The PAR-2-activating peptide H-Ser-Leu-Ile-Gly-Arg-Leu-NH2 (SLIGRL-NH2) induced eosinophil recruitment whereas PAR-2 blockade inhibited ovalbumin (OVA)- or CCL11-induced eosinophil recruitment. Moreover, OVA and CCL11 induced PAR-2 expression in pleural leukocytes, and the MC tryptase inhibitor APC 366 ([N-(1-hydroxy-2-napthoyl)-l-arginyl-l-prolinamide hydrochloride]) abolished CCL11-induced eosinophil recruitment. These results suggest a pro inflammatory effect of PAR-2 and support a role for MC tryptase mediating eosinophil migration via PAR-2 signaling. Taken together, our results suggest that PAR-2 activation through endogenous MC tryptase activity could be required, at least partially, to mediate CCL11-induced eosinophil migration.
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