human betaamyloid protein 42 (17)

Activated Protein C (390-404), human acetate (Activated Protein C ) inhibits APC anticoagulant activity.

Amyloid β Peptide (42-1)(human) acetate is the inactive form of Amyloid β Peptide (1-42). Amyloid β Peptide (42-1)(human) acetate is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease.

β-Amyloid (1-42), acetate (human) is a peptide consisting of 42 amino acids that is part of β-Amyloid and is commonly used in Alzheimer's disease modeling.

Apelin-17 (human, bovine) acetate is an endogenous apelin receptor agonist. Potently inhibits forskolin-stimulated cAMP accumulation (pIC50 = 9.94).

β-Amyloid precursor protein (96-110), cyclized (human), a segment of the amyloid precursor protein, serves as a research tool in Alzheimer’s disease studies [1].

PTH-Related Protein (1-37) (human, mouse, rat) is a peptide analog of parathyroid-hormone-related protein (pTHrP), which plays a role in the physiological regulation of bone formation [1].

Acetyl-Heme-Binding Protein 1 (1-21) (human) is a short peptide comprising the initial 21 amino acids of the hemopexin Acetyl-Heme-Binding Protein 1, which is involved in heme binding, heme metabolism, and the release of hemoglobin [1].

Tau protein (592-597), Human (TFA) is a peptide fragment of human Tau protein.

GIP (3-42), human acetate is an antagonist of a glucose-dependent insulinotropic polypeptide (GIP) receptor and regulates insulin secretion and GIP metabolism in vivo.

Agouti-related Protein (AGRP) (83-132) Amide (human) is a segment derived from the agouti-related protein (AGRP), abundantly present in the hypothalamus' arcuate nucleus. It predominantly functions as an inverse agonist for the melanocortin-4 receptor (MC4R), thereby promoting food intake [1] [2].

(Asn10,Leu11,D-Trp12)-pTH-Related Protein (7-34) amide (human, mouse, rat) is a potent antagonist of the PTH-1R [1] [2].

Human PTHrP-(1-34)NH2, also known as PTH-Related Protein (1-34) amide for human, mouse, and rat, is the N-terminal fragment of PTHrP. This peptide induces hypercalcemia and is utilized in the study of humoral hypercalcemia of malignancy [1].

Amyloid β-Protein (3-42), the precursor of Pyr peptide, serves as the foundation of the amyloid template block in Alzheimer's disease when modified to pyroglutamate Aβ (pEAβ) (3-42). This modified form, pEAβ(3-42), hastens the aggregation of Aβ(1-42) although Aβ(1-42) markedly decelerates both the primary and secondary nucleation of pEAβ(3-42) [1].

PTH-Related Protein (7-34) amide (human, mouse, rat) serves as a potent antagonist of parathyroid hormone (PTH) [1].

FITC-β-Ala-Amyloid β-Protein (1-42) ammonium, a fluorescein isothiocyanate (FITC)-tagged monomer peptide of Aβ1-42, is instrumental in Alzheimer’s disease pathogenesis [1].

GIP (3-42), human (Gastric Inhibitory Polypeptide (3-42) (human)) is a peptide that acts as a glucose-dependent proinsulinotropic polypeptide (GIP) receptor antagonist and regulates insulin secretion and the metabolic effects of GIP in vivo, which can be used to study type 2 diabetes.

β-Amyloid(17-28) human is a fragment of the β-amyloid peptide (Abeta) associated with Alzheimer's disease (AD), promoting the aggregation of the full-length β-Amyloid40 into toxic aggregates [1]. This lipid-induced amyloid core segment is implicated in AD pathogenesis.

β-Amyloid (42-1), human is the inactive form of Amyloid β Peptide (1-42) which plays a key role in the pathogenesis of Alzheimer disease.

Biotin-β-Amyloid (1-42), human TFA, also known as Biotin-Amyloid β-Peptide (1-42) (human) TFA, is a biotin-labeled 42-amino acid peptide implicated in the pathogenesis of Alzheimer's disease [1].

Gastric inhibitory peptide 1 (GIP-1) (3-42), a fragment of the incretin hormone GIP and antagonist to the GIP receptor, is generated through the action of serum dipeptidyl peptidase 4 (DDP-4). When administered at 25 nmol/kg to an ob/ob mouse diabetes model, GIP-1 (3-42) elevates plasma glucose levels and lowers plasma insulin levels, demonstrating its effect on reducing insulin secretion from BRIN-BD11 pancreatic cells at a concentration of 100 nM.

Cys-Gly-Lys-Arg-Amyloid β-Protein (1-42), a peptide fragment derived from amyloid β-protein (Aβ), plays a pivotal role in Alzheimer's disease research [1].

(Nle35)-Amyloid β-Protein (1-42) ammonium is a peptide.

Apelin-17(human, bovine) TFA is an endogenous agonist of the orphan G protein-coupled receptor APJ. This compound demonstrates affinity for human APJ receptors on HEK 293 cells, evidenced by a pIC50 value of 9.02. Additionally, Apelin-17(human, bovine) TFA has been shown to block the entry of certain HIV-1 and HIV-2 strains into NP2/CD4 cells that express the APJ receptor [1] [2] [3].

β-Amyloid (42-1), human TFA, a 42-amino acid peptide, represents the inactive form of Amyloid β Peptide (1-42) and is pivotal in the development of Alzheimer's disease [1].

(Gly22)-Amyloid β-Protein (1-42), a peptide fragment of Amyloid β-Protein (Aβ), plays a crucial role in Alzheimer's disease by forming the main component of both vascular and parenchymal amyloid deposits. The mutation from Glu22 to Gly22 in Aβ is known to enhance aggregation [1] [2].

'(Lys22)-Amyloid β-Protein (1-42) represents a mutation of the wild-type (WT) Amyloid β-Protein (1-42) peptide [1].'

β-Amyloid (1-42), human is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease.

Endogenous apelin receptor agonist. Potently inhibits forskolin-stimulated cAMP accumulation (pIC50 = 9.94).

Activated Protein C (390-404), human, a peptide derived from the vitamin K-dependent serine protease, effectively suppresses the anticoagulant activity of APC[1].

Biotinyl-Ahx-Amyloid β-Protein (1-42) ammonium is an N-terminally biotin-tagged form of Amyloid β-Protein (1-42), which constitutes the main component of vascular and parenchymal amyloid deposits associated with Alzheimer's disease [1].

(Met(O2)35)-Amyloid β-Protein (1-42) is a peptide [1] .

(Met(O)35)-Amyloid β-Protein (1-42) represents the oxidized form of Methionine 35 in Aβ42, capable of producing an oligomer size distribution akin to that of Aβ40. This compound is utilized in Alzheimer’s disease (AD) research [1].

(Gln22)-Amyloid β-Protein (1-42), a Dutch mutation (E22Q) variant of β-Amyloid (1-42), demonstrates increased fibrillogenic and pathogenic characteristics [1].

'(Tyr36)-pTH-Related Protein (1-36) (human, mouse, rat), a peptide, functions as a ligand for parathyroid hormone (PTH) receptors [1].'

Human Papillomavirus (HPV) E7 protein (49-57) is the H-2d-restricted human papillomavirus (HPV) E749-57 epitope.

(Glu20)-Amyloid β-Protein (1-42) represents a variant of amyloid β-protein (Aβ) that fibrillizes more slowly. This is attributed to the Glu20 mutation, which diminishes Aβ42's tendency to aggregate and inhibits the accumulation of this slowly fibrillizing peptide. Notably, amyloid β-protein serves as the principal constituent of amyloid deposits found in both the vascular system and brain parenchyma in Alzheimer's disease [1] [2].

(D-Asp1)-Amyloid β-Protein (1-42), a peptide fragment of amyloid β-protein (Aβ), serves as the primary constituent of vascular and parenchymal amyloid deposits associated with Alzheimer's disease [1].

[Tyr0] Gastric Inhibitory Peptide (23-42), human, functions as a glucose-dependent insulinotropic polypeptide (GIP) and exhibits dual activity: it modestly inhibits gastric acid secretion while simultaneously enhancing insulin secretion. This characteristic makes it applicable in research related to diabetes and obesity [1] [2].

pTH-Related Protein (1-40) (human, mouse, rat) enhances calcium absorption in rat intestinal cells by activating the PTHR1 receptor and the PKCα/β signaling pathways. This compound also increases the expression of the parathyroid hormone 1 receptor (PTHR1) and four key proteins involved in transcellular calcium transport: potential vanillin member 6 (TRPV6), calcium-binding protein-D9K (CaBP-D9k), sodium-calcium Exchanger 1 (NCX1), and plasma membrane calcium ATPase 1 (PMCA1) [1].

Agouti-related peptide (AgRP) is a neuropeptide produced in the brain by the AgRP/NPY neuron. It is only synthesized in NPY containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus. The appetite-stimulating effect

Amyloid 17-42 (Aβ(17-42)), a significant component of diffuse plaques in Alzheimer's disease and cerebellar pre-amyloid in Down's syndrome, results from the alpha- and gamma-secretase cleavage of amyloid precursor protein (APP). It has the capability to trigger neuronal apoptosis through the Fas-like/caspase-8 activation pathway [1].

Amyloid β-Protein (33-42) TFA, a fragment encompassing residues 33-42 of the β-amyloid protein, mitigates the toxicity induced by Aβ42 [1].

Biotinyl-Amyloid β-Protein (1-42) ammonium, a biotinylated variant of Amyloid β-Protein (1-42), is utilized in research focused on the conversion of Aβ1-42 to Aβ1-40 in the brain [1].

Amyloid β-Protein (36-42), the 36-42 fragment of β-Amyloid, consists of a polypeptide chain of 36-43 amino acids and is a primary constituent of amyloid plaques in Alzheimer's disease (AD) patients' brains. β-Amyloid oligomers (Aβos) critically contribute to AD progression by causing neuronal harm and cognitive decline [1].

'(Asp37)-Amyloid β-Protein (1-42) [1]' refers to the G37D mutant variant of the wild-type Amyloid-beta (1-42) peptide.

The peptide region containing residues 390-404 in Activated Protein C (APC) is essential for anticoagulant activity and is available for interaction with antibodies or with other proteins, such as the macromolecular substrates Factors Va or VIIIa. APC reg

Prion peptide fragment that exhibits neurotoxicity

β-Amyloid (1-42), (rat/mouse) (TFA) is a peptide fragment consisting of 42 amino acids that can be used to study Alzheimer's disease.