L-Homocarnosine free base

• CAS: 3650-73-5
• Catalog Number: ACM3650735
• Category: Main Products
• Molecular Weight: 0
• Molecular Formula: C₁₀H₁₆N₄O₃
• Synonyms: L-HOMOCARNOSINE FREE BASE;N-(4-amino-1-oxobutyl)-L-Histidine;γ-Aminobutyryl-L-histidine;Nα-(4-Aminobutyryl)histidine;γAbu-L-His-OH;L-Histidine, N-(4-aMino-1-oxobutyl)-
• IUPAC Name: (2S)-2-(4-aminobutanoylamino)-3-(1H-imidazol-5-yl)propanoicacid
• SMILES: C1=C(NC=N1)CC(C(=O)O)NC(=O)CCCN
• InChI Key: CCLQKVKJOGVQLU-QMMMGPOBSA-N
• Boiling Point: 646.9ºC at 760mmHg
• Flash Point: 345.1ºC
• Exact Mass: 240.12200
• WGK Germany: 3

Case Study

L-Homocarnosine-Containing HCA Supplement: Neuroprotection in a PTZ-Induced Seizure Model (OVX Rats)

Qi, Ziyou, et al. 3 Biotech 8.8 (2018): 363.

A preclinical research team evaluated a combined supplement containing L-homocarnosine, L-carnosine, and anserine (referred to hereafter as HCA) to assess its ability to reduce seizure-related oxidative damage and enhance anticonvulsant responses. The work used a pentylenetetrazole (PTZ) seizure model in female rats, including ovariectomized (OVX) animals, to mimic hormone-depleted conditions that can influence brain oxidative stress.
Key Findins:
· Effect of HCA supplementation: OVX animals showed significant alterations in biochemical markers indicating elevated oxidative stress. Combined HCA treatment significantly reduced lipid peroxidation and increased GSH, Gpx, SOD, catalase, and thiol levels in PTZ-treated OVX rats compared with untreated PTZ groups.
· Anticonvulsant activity: Ovariectomy itself produced an elevation in latency to GTCS. HCA supplementation substantially increased latency to both minimal clonic seizures and GTCS in OVX+PTZ and sham+PTZ groups, consistent with enhanced anticonvulsant activity.
· Combined HCA supplementation was associated with both biochemical evidence of reduced oxidative damage and improved seizure latency metrics in this PTZ seizure model.

L-Homocarnosine: Mitigating Inflammation and Tissue Damage after Cerebral Ischemia-Reperfusion

Huang, Jing, et al. International Journal of Biological Macromolecules 118 (2018): 357-364.

Oxidative and inflammatory processes are deeply involved in the development of secondary brain damage, such as those that take place in ischemia-reperfusion injury (IRI) after a stroke. The NLRP3 inflammasome is a key mediator of this harmful inflammatory response. The effects of L-homocarnosine were tested in a rat model of middle cerebral artery occlusion (MCAO) to induce cerebral IRI. The treatment groups received 0.5 mM and 1 mM of L-homocarnosine in addition to the MCAO procedure.
Administration of L-homocarnosine demonstrated significant protective effects across multiple parameters:
· Enhanced Antioxidant Capacity: Compared to MCAO control group, animals treated with L-homocarnosine had significant increases in the levels of antioxidant enzymes (SOD, catalase, Gpx) and reduced glutathione (GSH), along with a significant reduction in the levels of lipid peroxidation.
· Improved Neurological and Structural Outcomes: L-Homocarnosine treatment reduced the cerebral infarct area, lowered neurological deficit scores, and diminished histopathological signs of apoptosis and necrosis in brain tissue.
· Reduction of the mRNA expression of pro-inflammatory markers NLRP3, TNF-α, and IL-6. All three were found to be increased in the MCAO rats. L-Homocarnosine significantly reduced (by over 40%) the mRNA expression of these three factors. NLRP3 protein expression was reduced by over 30% in the 1 mM L-Homocarnosine treatment group.

L-Homocarnosine as an Adjunct to Vancomycin in a Rat Model of Staphylococcus aureus Osteomyelitis

Zhou, Panyu, et al. Biomedicine & Pharmacotherapy 111 (2019): 31-35.

This experiment assessed L-homocarnosine as both monotherapy and in combination with the antibiotic vancomycin, in a rat model of S. aureus osteomyelitis. The five treatment groups were vehicle (sham), infected control, vancomycin, L-homocarnosine, and vancomycin + L-homocarnosine. For the three active treatment groups the doses were 25 mg/kg body weight for each agent.
Results of the vancomycin + L-homocarnosine combination group were superior to monotherapy:
· Oxidative stress and antioxidant enzymes: Combined vancomycin + L-homocarnosine treatment reduced lipid peroxidation (MDA) by more than 50% and restored catalase, SOD, Gpx and GSH to near-normal levels. Vancomycin or L-homocarnosine alone produced smaller improvements.
· Inflammatory cytokines: Control (infected) animals had elevated TNF-α (6.3 U/mL) and IL-6 (7.3 U/mL). The combination therapy significantly lowered TNF-α and IL-6 to near-normal values, outperforming either monotherapy.
· Vancomycin alone produced only marginal reductions in bacterial growth at 72 h; L-homocarnosine alone produced a slight reduction. The combined treatment significantly reduced bacterial counts on both bone and wire relative to control.
· Severe bone infection and higher histopathological scores were evident in controls. Monotherapies yielded modest reductions in lesion severity, while the vancomycin + L-homocarnosine group showed a significant reduction in bone infection and histopathological score. Body weights (mean at 72 h): Group I 184.6 g (sham), Group II 165.7 g (control), Group III 197.5 g (vancomycin), Group IV 193.4 g (L-homocarnosine), Group V 205.7 g (combination).