Péptidos

Peptide Ac-TNL-NH2 is a Research Peptide with significant interest within the field academic and medical research. This peptide is available for purchase at Cymit Quimica in multiple sizes and with a specification of your choice.

Custom research peptide; min purity 95%. For different specs please use the Peptide Quote Tool

Acetylated α-synuclein (1-7) amide is derived from the alpha-synuclein intrinsically disordered protein which is found in the neurons and presynaptic terminals. Encoded by the SNCA1/PARK1 gene alpha-synclein is structurally composed of 140 amino acids, making up the three domains: N-terminal membrane binding domain, a hydrophobic non-amyloid-β component domain and a hydrophilic C-terminal domain. Usually alpha-synuclein plays a role in protecting neurons from apoptotic stimuli and is involved in synaptic vesical trafficking.However it has been found that the accumulation of alpha-synuclein aggregates can lead to neurodegenerative diseases such as Parkinson disease, dementia with Lewy bodies and multiple system atrophy. It is further involved in the fibrilisation of amyloid-b and tau which play a major role in Alzheimer disease. Amyloid fibrils are formed from alpha synuclein monomers within the cytosol and when bound to membranes these monomers can undergo conformational changes to form protofibrils and then ring like oligomers. This can result in the formation of transmembrane pores which disrupts the membrane, calcium homeostasis and signalling.Alpha-synuclein can be subjected to the post-translational modifications of phosphorylation and N-terminal acetylation. When acetylation occurs at the N-terminus of an alpha-synuclein monomer, the intramolecular hydrogen bonds are altered thus reducing the rate of alpha-synuclein aggregation and the strength at which it interacts with the membrane is increased.

Amyloid β-peptide (Aβ) has been identified as the key subunit of the extracellular plaques found in the brains of patients with Alzheimer's disease (AD) and Down's syndrome (DS). Aβ has therefore been extensively studied as a potential target for treatment of AD. Aβ is formed from the cleavage of the large, transmembrane protein- APP (amyloid precursor protein). Cleavage of APP by β- and then γ-secretases results in the formation of Aβ. Aβ can aggregate to produce amyloid-β oligomers, which are thought to be highly neurotoxic. Over time Aβ can further aggregate to produce the characteristic senile plaques present in AD and DS. Aβ can be degraded by enzymes such as neprilysin, insulin degrading enzyme or endothelin converting enzyme. At physiological levels Aβ may be involved in controlling synaptic activity and neuronal survival.

SARS-CoV-2 NSP7 (1-15)

Small peptide design has become of interest to catalyse chemical transformations within the cell. The aim is to generate peptides to enhance the hybridization of attached oligonucleotides to complementary DNA sequences. (AAKK)4 is modelled on the surface of staphylococcal nuclease, it a short cationic lysine-rich peptide that can deliver a nucleophile to DNA or RNA. (AAKK)4 peptide can improve DNA-PNA (peptide nucleic acid) hybridisations dramatically as well as increase strand invasion rate. (AAKK)4 peptide is a non-lipid approach for cell penetration which is preferable for certain cell lines due to cytotoxicity issues. (AAKK)4-antisense conjugates have been used to silence gene expression.(AAKK)4 is provided here with a N-terminal alkyne attachment. Two of the most regularly encountered functional groups for click chemistry are azides and alkynes, and the azide-alkyne cycloaddition has become the most popular click reaction. The use of click chemistry with alkyne-(AAKK)4 allows a wide variety of applications particularly for conjugation, modification, and peptide design.

Peptide Ac-CR-NH2 is a Research Peptide with significant interest within the field academic and medical research. This peptide is available for purchase at Cymit Quimica in multiple sizes and with a specification of your choice.

Galanin (1-30) (human) is an endogenous neuropeptide with endocrine, metabolic and behavioural effects. Galanin has a role in intestinal smooth muscle contraction, insulin and somatostatin release, and synaptic neurotransmission.Galanin is widely distributed in the central nervous, peripheral, and endocrine systems. Galanin's overarching function is as an inhibitory, hyper-polarizing neuromodulator for classical neurotransmitters like acetylcholine and serotonin. Galanin interacts with 3 receptor subtypes, GalR1-3 G protein-coupled receptors inserted into the plasma membrane. GalR1 is believed to activate a Gβγ pathway to regulate MAPK activation. GalR2 can also activate the MAPK pathway, but unlike GalR1, there is detectable inositol phosphate production. GalR3 is associated with the Galphai/o pathway. Activation of the receptor leads to a cellular influx of K+. Each receptor has been associated with neurological diseases such as GalR3 and epilepsy.Galanin protects against various physiological insults in vitro, including excitotoxicity and β-amyloid toxicity. Changes in galanin have been widely studied concerning Alzheimer's disease, and galaninergic neurons are spared in late-stage Alzheimer's relative to non-galaninergic neurones.Galanin (1-30) has been used as an agonist for the GalR2 receptor in vitro for calcium mobilisation assays to understand the role Galanin/GalR2 play in multiple sclerosis.Galanin (1-30) is provided with an N-terminal 5-TAMRA, a widely used red fluorescent reagent ideal for peptide labelling and detection. The excitation/emission for this reagent is 555 nm/580 nm.

Histone 3 (H3) is one of the four core histones (H2A, H2B, H3 and H4) fundamental in compacting eukaryotic DNA into the nucleosome. The nucleosome arises when 147 base pairs of DNA wrap around a H3-H4 tetramer and two H2A-H2B dimers, forming the histone octamer core. Similar to the other core histone, H3 has a globular domain and a flexible N-terminal domain, 'histone tail' which can undergo modifications such as acetylation, methylation, phosphorylation and ubiquitination. The transcriptional activation or silencing of the chromatin is controlled by ATP-dependent chromatin remodelling factors and histone modifying enzymes which target histone proteins. Both processes function to alter the positioning of the nucleosome, allowing the DNA it to be either available or inaccessible to the transcription machinery.The lysine at position 4 of this peptide has been tri-methylated and it is implicated in studies that this modification may remodel the chromatin so that it is more accessible to transcription factors, which may ultimately increase the level of gene expression. Moreover, the serine at position 10 has been phosphorylated, and studies have suggested that this may induce chromatin condensation, and subsequently repress transcription and gene expression.Histone H3 (1-20) K4Me3, pS10-GG-[Lys(5-FAM)] has a C-terminal GKK linker labelled with 5-Carboxyfluorescein (5-FAM), a widely used green fluorescent tag.

Protease activated receptors (PARs) are a distinctive four-member family of seven transmembrane G protein-coupled receptors (GPCRs) widely expressed in inflammatory cells. PARs are cleaved by certain serine proteases to expose a tethered ligand domain, this ligand domain then binds to and activates the receptors to initiate multiple signalling cascades. These PAR-activating proteases therefore represent PAR agonists. This PAR-2 agonist peptide mimics the sequence of the 'tethered ligand' and is therefore capable of activating the receptor independently of N-terminal proteolysis.SLIGRL-NH2 inhibits the development of airway eosinophilia, hyper-responsiveness and displays bronchodilator activity in allergic mice and also facilitates gastrointestinal transit in mice-in vivo.PAR activation has been linked to inflammation, therefore compounds that mimic or interfere with the PAR-activating processes are attractive therapeutic candidates.

Angiotensin-IV is primarily produced from angiotensin-III by the removal of an arginine residue from the N-terminal by membrane alanyl aminopeptidase N (AP-N). Ang-IV can however also be formed by the action of aminopeptidases on Ang-I directly.Ang-IV has been shown to enhance cognitive functions, although how it does this in still unclear. It has been suggested that Ang-IV is able to inhibit the insulin-regulated aminopeptidase (IRAP) receptor in the brain (originally defined as the AT(4) receptor). IRAP is a single-spanning transmembrane zinc-metallopeptidase that belongs to the M1 family of aminopeptidases and its substrates include vasopressin, somatostatin, and cholecystokinin. The half-life of these compounds are prolonged when IRAP is inhibited by Ang-IV, and this may result in the enhanced cognitive abilities seen with Ang-IV treatment. c-Met, a tyrosine kinase receptor that binds hepatocyte growth factor (HGF) has also been proposed as an Ang IV targets. c-Met is associated with memory and learning consolidation.

Acetylated α-synuclein (1-13) is derived from the alpha-synuclein intrinsically disordered protein which is found in the neurons and presynaptic terminals. Encoded by the SNCA1/PARK1 gene alpha-synclein is structurally composed of 140 amino acids, making up the three domains: N-terminal membrane binding domain, a hydrophobic non-amyloid-β component domain and a hydrophilic C-terminal domain. Usually alpha-synuclein plays a role in protecting neurons from apoptotic stimuli and is involved in synaptic vesical trafficking.However it has been found that the accumulation of alpha-synuclein aggregates can lead to neurodegenerative diseases such as Parkinson disease, dementia with Lewy bodies and multiple system atrophy. It is further involved in the fibrilisation of amyloid-b and tau which play a major role in Alzheimer disease. Amyloid fibrils are formed from alpha synuclein monomers within the cytosol and when bound to membranes these monomers can undergo conformational changes to form protofibrils and then ring like oligomers. This can result in the formation of transmembrane pores which disrupts the membrane, calcium homeostasis and signalling.Alpha-synuclein can be subjected to the post-translational modifications of phosphorylation and N-terminal acetylation. When acetylation occurs at the N-terminus of an alpha-synuclein monomer, the intramolecular hydrogen bonds are altered thus reducing the rate of alpha-synuclein aggregation and the strength at which it interacts with the membrane is increased.

This anti-microbial peptide (AMP) has been shown to cause lysis of several human cancer cell lines. Macropin-2 is most potent against CCRF-CEM T lymphoblastoid (human acute lymphoblastic leukemia) cells. At higher concentrations Macropin-2 also causes lysis of human umbilical vein endothelial cells (HUVEC), rat intestinal epithelial cells (IEC), human cervix carcinoma (HeLa) cells and human colon adenocarcinoma (SW480). Macropin-1 is also available in our catalogue.

Broad-spectrum antibacterial, active against multidrug-resistant Gram-negative bacteria. Acts though permeabilizing the bacterial membrane and also shows anti-inflammatory activity via a TLR4-mediated NF-KB signaling pathway. Significantly improves survival in a mouse sepsis model.

Vasoactive intestinal peptide (VIP) is a neuropeptide found throughout the body and the central nervous system (CNS). VIP is located within cell bodies and nerve endings of the enteric nervous system, brain and pancreas. VIP neurons in the peripheral system fire to regulate blood vessels, and the  CNS innervate cerebral vasculature. VIP  binds to G protein-coupled receptors VPAC1 and VPAC2. VIP and VPAC2 are detected in circular smooth muscle cells of cerebral arterioles. VIP and VPAC1 are also found in lymphatic tissue. VIP can block inflammation, modify the Th response favouring Th2 and induce regulatory T cells. Overexpression of each receptor has been linked to various cancers.VIP administration leads to pancreatic bicarbonate-rich fluid secretion but not to the same degree stimulated by secretin. VIP stimulates insulin secretion in a glucose-dependent manner and also stimulates glucagon secretion. Studies have found that in morbidly obese patients, VIP levels are lowered and work to slow gastric and duodenal motility but increase gastric emptying. Therefore, decreasing VIP levels in obese patients may increase weight gain by accelerating gastric emptying.VIP has been well studied in pancreatic acini. VIP is a full agonist of amylase secretion and increases cyclic AMP synchronised with an increase in intracellular Ca2+ triggered by stimuli that act through cholecystokinin (CCK) or cholinergic agonists. Most cAMP increases, and amylase secretion appear to be mediated via VPAC1.The discovery of VPAC antagonists can help to understand VIPs roles and may also provide new therapies in VIP dysregulated systems such as cancers. VIP (6-28) is a specific competitive inhibitor of the VIP receptor derived from VIP. VIP-induced vasodilatation was blocked by co-administration of the VIP receptor antagonist VIP (6-28). Using a VIP receptor antagonist has made VIP function easier to study during neuronal injury, inflammation, and heart innervation. The VIP receptor antagonist is being considered for osteoarthritis treatment, an area with no current treatments other than analgesics.

LL-37 is a member of the large cationic family of anti-microbial peptides called cathelicidins which have broad-spectrum anti-microbial activity and are expressed in many species. The only cathelicidin found in humans is LL-37, this is produced in epithelial cells, by proteolytic cleavage from the C-terminal of the hCAP-18 protein. LL-37 can be processed into different forms of anti-microbial peptides. As well as its anti-microbial properties LL-37 also regulates many aspects of the innate immune system and overexpression of LL-37 has been linked to autoimmune diseases such as asthma and psoriasis, making LL-37 the most studied form of the human cathelicidin peptides.More recently, studies have shown that LL-37 binds to SARS-CoV-2 S protein and inhibits binding to its receptor hACE2, which may inhibit viral entry into the cell. LL-37 is upregulated by vitamin D, therefore this may be one mode of action for the positive outcomes seen with vitamin D treatment for Covid-19.

Peptide Ac-TGGKAPR-NH2 is a Research Peptide with significant interest within the field academic and medical research. This peptide is available for purchase at Cymit Quimica in multiple sizes and with a specification of your choice.

Membrane-active peptide that binds to HDM-2 expressed in the membranes of solid tissue tumour cells to induce transmembrane pore formation in cancerous, but not normal cells, resulting in tumour cell necrosis independent of p53 activity.

TP10 is an amphipathic cell-penetrating peptide (CPP) also known as transportan 10. Its formation involves the use of a lysine residue to form a chimeric linkage between a mastoparan 21-residue peptide, a wasp venon 14-residue peptide and 6-residues derived from the neuropeptide galanin. Structurally TP10 contains only positively charged amino acids along with 4 lysines and an N-terminus. Therefore, it will produce a +5 charge under conditions of a neutral pH. It has been found that TP10 may aid molecules in penetrating through the cell membrane barrier through directly interacting with the lipid bilayer. During these interactions with the membrane TP10 will form an amphipathic α-helix. TP10 can be used in transduction methods.TP10 is provided here with a N-terminal alkyne attachment. Two of the most regularly encountered functional groups for click chemistry are azides and alkynes, and the azide-alkyne cycloaddition has become the most popular click reaction. The use of click chemistry with alkyne-TP10 allows a wide variety of applications particularly for conjugation, modification, and peptide design. Fluorescent labelling of TP10 for drug delivery has been used in vivo.

IRBP (1-20) is derived from the interphotoreceptor retinoid-binding protein (IRBP), present in the interphotoreceptor matrix and is expressed by cone and rod photoreceptors in the eye. IRBP is involved in retinoid delivery and protects retinal cells from oxidative stress.In retinitis pigmentosa patients, IRBP can be subjected to mutations resulting in a non-secreted form of IRBP to be produced. Furthermore IRBP gene mutations have been associated with high myopia and retinal dystrophy.The expression of IRBP is reduced in diabetes patients which may lead to visual cycle misfunction and the photoreceptors can be vulnerable to damage.

RAGE antagonist peptide is an S100P-derived peptide based competitive antagonist for receptor for advanced glycation end product (RAGE). Recent studies have shown it to disrupt the interaction between RAGE and its ligands, such as S100P, S100A4 and HMGB-1 in binding assays and in multiple cancer cell lines. As well as this, it also blocks RAGE-dependent NF-kB activation in MPanc96, MOH and HPAF II tumor cell lines.Systemic administration of RAGE antagonist peptide also diminishes NF-kB signaling in vivo and significantly reduces glioma tumour growth in murine models.

LHRH.

Duchenne muscular dystrophy is a severe muscle wasting X-linked genetic disease cause by mutations in the gene encoding the muscle structural protein, dystrophin. Exon skipping therapy remains a key approach for treatment of DMD but still requires considerable research to improve efficient and specific delivery of molecules to myofibers. Use of a phage library identified this sequence as having a high affinity for myofibers. Conjugation of this peptide to novel DMD molecules could provide the insights needed in the field.

Peptide identified through phage display that binds to colorectal cancer cell line RKO cells, as well as other cancer cells including Caco-2, HCT 116 and HCT-15, but not to normal cells, possibly through targeting the monocarboxylate transporter 1, which has been implicated in colorectal cancer progression and prognosis.

GIP (1-30) Human amide is derived from the Gastric inhibitory peptide (GIP). Gastric inhibitory polypeptide (GIP) is an inhibiting hormone of the secretin family of hormones. While GIP is a weak inhibitor of gastric acid secretion, its main role is to stimulate insulin secretion - in a glucose-dependent mechanism. Therefore, GIP is referred to as a glucose-dependent insulinotropic peptide.GIP is derived from a 153-amino acid pro-protein encoded by the GIP gene. It is synthesised by K cells, which are found in the mucosa of the duodenum and the jejunum of the gastrointestinal tract. GIP receptors are seven-transmembrane proteins found on β-cells in the pancreas. These β-cells are those that are able to simultaneously detect glucose and release insulin as a result to GIP binding.The clinical relevance of GIP is related to type 2 diabetes mellitus (T2DM)- studies have found that T2DM diabetics are unresponsive to GIP and have lower levels of GIP secretion after a meal when compared to non-diabetics. In research involving knockout mice, it was found that absence of the GIP receptors correlates with resistance to obesity.

[β-Ala]-[Lys(AMCA)]-acid.

PDGF-Ra agonist with in vitro and in vivo antimelanoma growth activity.

HPV16 E6 pep11**m.