Death

Programmed cell death in bacteria is dependent on a system of cell-to-cell communication termed quorum sensing. Extracellular death factor (EDF) is a linear pentapeptide that communicating cells produce and release, which upon reaching a sufficient concentration activates the cell death pathway in a subset of cells. It is sensitive to extreme pH, high temperatures, and other stressful conditions. At 2.5 ng/ml, EDF has been shown to facilitate mazEF-mediated cell death, significantly reducing population size in E. coli cultures.

Extracellular Death Factor TFA (EDF TFA) is a linear pentapeptide that is produced and released by communicating cells and activates cell death pathways in cellular subpopulations when sufficient concentrations are reached.EDF TFA is sensitive to extreme pH, high temperatures, and other stressful conditions. At a concentration of 2.5 ng/ml, EDF has been shown to promote mazeEF (toxin-antitoxin system within bacteria) mediated cell death, promote the endonuclease activity of MazF toxin, lead to degradation of bacterial mRNA, and significantly reduce population size in E. coli cultures.

BzATP triethylammonium salt is a P2X7 receptor agonist.

Peptide5 acetate reduces animal swelling, astrogliosis, and neuronal cell death after spinal cord injury. Peptide5 acetate significantly reduces the degree of spinal cord injury (SCI) in a rodent ex vivo model.

Calcineurin Autoinhibitory Peptide acetate is a selectivecalcineurin phosphatase inhibitor(IC50 ~ 10 μM). Calcineurin Autoinhibitory Peptide acetate can be used in the protection of neurons from excitatory neuronal death.

α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937 cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)

Epsilon-V1-2 has been extensively investigated for its function as a PKC epsilon (PKCε) inhibitor. Epsilon-V1-2 has been widely applied in studies addressing ovarian aging, apoptosis in human granulosa cells, cerebral ischemia-reperfusion injury, brain development, hepatocyte insulin signaling, and neuronal cell death under ischemic conditions. Epsilon-V1-2 has been shown to effectively reduce PKCε activity, thereby enabling detailed exploration of regulatory pathways involving mitochondrial dynamics, calcium overload, AKT activation, brain atrophy, insulin resistance, and ferroptosis. Epsilon-V1-2 demonstrates notable therapeutic relevance in models of stroke, SHORT syndrome, hepatic steatosis, and brain injury, supporting its continued evaluation as a potential pharmacological agent across multiple disease contexts.

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

Human PD-L1 inhibitor III [Human PD-L1 inhibitor] is a bioactive compound designed to inhibit the programmed death-ligand 1 (PD-L1) protein in humans.

Ozarelix is a fourth generation GnRH antagonist, induces apoptosis in hormone refractory androgen receptor negative prostate cancer cells modulating expression and activity of death receptors. Mechanistically, LHRH antagonists exert rapid inhibition of luteinizing hormone and follicle stimulating hormone with an accompanying rapid decrease in sex hormones and would therefore be expected to be effective in a variety of hormonally dependent disease states including ovarian cancer, prostate cancer, BPH, infertility, uterine myoma and endometriosis. BPH is a non-cancerous enlargement of the prostate that is caused by testosterone. Unlike LHRH agonists, ozarelix has the potential to reduce testosterone just enough to reduce both prostate size and symptoms without the severe side effects associated with a reduction in testosterone.

Dalargin, a potent δ-opioid receptor agonist, demonstrates efficacy in mitigating cell death induced by Gentamicin and exhibits nephroprotective effects against Gentamicin-induced kidney injury. Additionally, Dalargin possesses antiulcer activity [1] [2] [3].

Calcineurin Autoinhibitory Peptide TFA is a selective inhibitor of Ca2+/calmodulin-dependent protein phosphatase (calcineurin), exhibiting an inhibitory concentration (IC50) of approximately 10 μM. This compound has been shown to protect neurons from excitatory neuronal death [1] [2].

Dynorphin A TFA, an endogenous opioid peptide, plays a role in inhibitory neurotransmission within the central nervous system (CNS). It acts as a highly potent kappa opioid receptor (KOR) agonist and also stimulates other opioid receptors, including mu (MOR) and delta (DOR). Furthermore, Dynorphin A TFA has been observed to induce neuronal death, making it a significant subject in neurological disease research [1] [2].

DAPK Substrate Peptide TFA is a synthetic peptide used as a substrate for the enzyme death-associated protein kinase (DAPK), with a Michaelis constant (Km) of 9 μM [1].

MDP1, derived from Melittin, disrupts the membrane integrity of both Gram-positive and Gram-negative bacteria, leading to bacterial death through membrane damage. This compound exhibits potent antibacterial activity against multidrug-resistant (MDR) and reference strains of S. aureus, E. coli, and P. aeruginosa [1].

MDP1 acetate, a derivative of Melittin, compromises the membrane integrity of both Gram-positive and Gram-negative bacteria leading to bacterial death through membrane damage. It exhibits potent antibacterial activity against multidrug-resistant (MDR) and reference strains of S. aureus, E. coli, and P. aeruginosa [1].

Leptin (116-130), a bioactive fragment of leptin, enhances synaptic plasticity in the hippocampus by promoting AMPA receptor trafficking to synapses. It preserves hippocampal synapse integrity and prevents neuronal cell death in amyloid toxicity models, showing promise for Alzheimer's disease (AD) research [1].

WL12 is a peptide that targets and binds specifically to programmed death ligand 1 (PD-L1). It can be radiolabeled with various radionuclides to produce radiotracers, enabling the evaluation of PD-L1 expression in tumors [1].

GPR, a tripeptide, shows promise in Alzheimer's disease (AD) research by protecting cultured rat hippocampal neurons from amyloid-beta (Aβ)-induced death through the inhibition of caspase-3/p53-dependent apoptosis.

GPR acetate (47295-77-2 Free base) is a tripeptide containing three amino acids that inhibits caspase-3/p53-dependent apoptosis mechanisms, protecting cultured rat hippocampal neurons from Aβ-induced death. It is suitable for Alzheimer's disease (AD) research.

Pinealon is a 3-amino acid peptide that shows neuroprotective properties by preventing reactive oxygen species (ROS) accumulation and suppressing the activation of ERK 1/2. Pinealon stimulates the functional activity of the main cellular elements of brain tissue, reduces the level of spontaneous cell death, and protects rat offspring from prenatal hyperhomocysteinemia [1] [2] [3].

Ac-Leu-Val-Lys-Aldehyde is a potent inhibitor of cathepsin B, with an inhibitory concentration (IC50) of 4 nM. It significantly reduces quinolinic acid-induced cell death in the striatum and results in the accumulation of LC3-II [1].

Peptide5 TFA, a connexin 43 mimetic peptide, mitigates swelling, astrogliosis, and neuronal cell death in animal models of spinal cord injury, and suppresses the NLRP3 inflammasome, functioning as an anti-inflammatory agent (1) (2) (3).

Ac-IETD-CHO is a potent, reversible inhibitor of granzyme B and caspase 8, which also impedes Fas-mediated apoptosis, hemorrhagic conditions, and liver failure. Furthermore, this compound hampers cell death induced by cytotoxic T lymphocytes [1] [2].