N-Oleoyl valine is an endogenous N-acyl amine that acts as an antagonist at the transient receptor potential vanilloid type 3 (TRPV3) receptor, which is involved in thermoregulation. N-Oleoyl valine is increased in mice following cold exposure for up to at least 16 days. Acute lung injury in mice increases the concentration of N-Oleoyl valine in lung tissue. N-acyl amines also promote mitochondrial uncoupling.
Aclerastide is an angiotensin receptor agonist. Administration of Aclerastide reduced fibrosis and scarring in the healing wounds. This action was more pronounced with longer administration of the peptide after injury. The action of this peptide was block
Pro-Adrenomedullin(153-185),human, (C143H224N42O43), a peptide with the sequence H2N-SLPEAGPGRTLVSSKPQAHGAPAPPSGSAPHFL-OH, MW= 3219.6. Adrenomedullin (AM) is a ubiquitously expressed peptide initially isolated from phaechromyctoma in 19931. AM was initially identified as a vasodilator, some have cited this as the most potent endogenous vasodilatory peptide found in the body2. Differences in opinion regarding the ability of AM to relax vascular tone arises from the differences in the model system used3. Other effects of AM include increasing the tolerance of cells to oxidative stress and hypoxic injury and angiogenesis. AM is seen as a positive influence in diseases such as hypertension, myocardial infarction, chronic obstructive pulmonary disease and other cardiovascular diseases, whereas it can be seen as a negative factor in potentiating the potential of cancerous cells to extend their blood supply and cause cell proliferation.
Antileukinate is a synthetic hexapeptide with an acetylated amino terminus and an amidated carboxyl terminus that inhibits the binding of CXC chemokines to the chemokine receptor CXCR2. It inhibits IL-8 binding to neutrophils (Ki = 2.7-13 μM), prevents neutrophil chemotaxis and β-glucuronidase release, and blocks IL-8-induced skin edema in rabbits. At 53 mg/kg, antileukinate has been shown to protect mice against acute pancreatitis and associated lung injury.
Connexin43 mimetic peptide. Reduces swelling, astrogliosis, neuroinflammation and neuronal cell death following spinal cord injury ex vivo and in vivo. Exhibits analgesic effects in models of neuropathic pain.
O'Carroll et al (2008) Connexin 43 mimetic peptides reduce swelling, astrogliosis and neuronal cell death after spinal cord injury. Cell.Commun.Adhes. 15 27 PMID:18649176 |Mao et al (2017) Characterisation of Peptide5 systemic administration for treating traumatic spinal cord injured rats. Exp.Brain.Res. 235 3033 PMID:28725925 |Kim et al (2017) Characterising the mode of action of extracellular Connexin43 channel mimetic peptides in an in vitro ischemia injury model. Biochem.Biophys.Acta. 1861 68 PMID:27816754 |Tonkin et al (2017) Attenuation of mechanical pain hypersensitivity by treatment with Peptide5, a connexin-43 mimetic peptide, involves inhibition of NLRP3 inflammasome in nerve-injured mice. Exp.Neurol. 300 1 PMID:29055716
Cyclo(L-Phe-L-Val) is a metabolite of the sponge bacterium Pseudoalteromonas sp. NJ6-3-1 that can autoinduce production of antibacterial substances active against S. aureus when co-cultured at a low cell density. It induces neurite outgrowth and branching of chick cortical neurons in vitro when used at concentrations of 16 and 32 μM. It increases phosphorylation of the PI3K substrate Akt, and neurite outgrowth induced by cyclo(L-Phe-L-Val) can be blocked by the PI3K inhibitor LY294002 . Cyclo(L-Phe-L-Val) enhances axon sprouting of calcitonin gene-related protein positive (CGRP+) primary afferents in the spinal cord following crush injury and of serotonin neurons in uninjured spinal cord. Cyclo(L-Phe-L-Val) is also a bitter taste component of cocoa and roasted coffee.
Z-LEHD-FMK TFA is a specific and irreversible inhibitor of caspase-9, offering protection against detrimental reperfusion injury and moderating apoptosis. Additionally, Z-LEHD-FMK TFA demonstrates its neuroprotective potential in a rat model of spinal cord trauma.