Peptides(肽)

Cat.No. 产品名称 Information

GA24030 (d(CH?)?¹,Tyr(Me)²,Dab?,Arg?,Tyr?)-Vasopressin

d(CH2)5[Tyr(Me)2,Dab5]-AVP

Replacement of Asn5 by isosteric Dab generates a vasopressin antagonist.

GA24031 (D-Ala¹?)-Liraglutide trifluoroacetate salt The peptide is an impurity of Liraglutide.

GA24032 (D-Arg?)-Inotocin

[D-Arg8]-Inotocin

Analog of the insect neuropeptide inotocin acting as human vasopressin V1a-receptor antagonist.

GA24033 (D-Cys?,des-L-threoninol?)-Octreotide Potential impurity of octreotide.

GA24034 (Deamino-Cys¹)-Oxytocin

dOT

Oxytocin analog with prolonged activity.

GA24038 (Deamino-Cys¹,β-cyclohexyl-Ala?,Dab?)-Vasopressin

d[Cha4,Dab8]-AVP

Introduction of Cha generates agonists for the human V1b receptor.

GA24035 (Deamino-Cys¹,Arg?)-Vasopressin

dAVP

(Deamino-Cys¹,Arg?)-Vasopressin is a used to treat diabetes insipidus, bedwetting, hemophilia A, von Willebrand disease, and high blood urea levels.

GA24036 (Deamino-Cys¹,Lys?)-Oxytocin

dOTK8

Desamino-LVT showed the oxytocic activity of Lysine-vasotocin without detectable pressor activity.

GA24037 (Deamino-Cys¹,Tyr(Me)²,Val?,D-Arg?)-Vasopressin

d[Tyr(Me2)]VdAVP

A highly specific and potent antidiuretic AVP agonist.

GA20094 (Des-Cys¹,cyclo(Ser²-Asu⁷))-Calcitonin (eel)

依降钙素

Elcatonin, also known as carbocalcitonin, is the aminosuberic acid analog of eel calcitonin. It has all the biological properties of the corresponding natural calcitonin (H-2255). The substitution of the disulfide bond of natural calcitonins with an ethylene bridge in 1-7 N-terminal position gives elcatonin greater stability and excellent tolerability when used in vivo.

GA20095 (Des-Glu²²)-Amyloid β-Protein (1-40) The Osaka mutation was the first deletion-type mutation to be identified in APP and Aβ. The Aβ E22delta mutant is more resistant to degradation by two major Aβ-degrading enzymes, neprilysin and insulin-degrading enzyme. Synthetic mutant Aβ showed unusual aggregation properties with enhanced oligomerization but no fibrillization. It also inhibited hippocampal long-term potentiation more efficiently than wild-type Aβ. A transgenic mouse model containing APP with the E693delta mutation has been developed. APP(OSK)-Tg mice exhibit intraneuronal Aβ E22delta oligomers and memory impairment as early as eight months of age.

GA20096 (Des-Glu²²)-Amyloid β-Protein (1-42) The Osaka (E22delta) mutation of Amyloid β promotes β-sheet transformation, radical production, and synaptotoxicity, but not neurotoxicity.

GA24039 (Des-Gly²?)-Liraglutide trifluoroacetate salt The peptide is an impurity of Liraglutide.

GA24040 (Des-Gly³¹)-Liraglutide trifluoroacetate salt The peptide is an impurity of Liraglutide.

GA24041 (Des-His¹)-Glucagon trifluoroacetate salt

Glucagon (2-29)

The peptide is an impurity of glucagon.

GA24042 (Des-L-threoninol?)-Octreotide amide Potential impurity of octreotide.

GC41699 (Des-octanoyl)-Ghrelin (human) (trifluoroacetate salt) A peptide hormone

GA24043 (Des-Ser?)-Liraglutide trifluoroacetate salt The peptide is an impurity of Liraglutide.

GA20182 (Gln²²)-Amyloid β-Protein (1-40) The Dutch mutation (E22Q) of amyloid β-peptide aggregates more readily than the wild-type peptide and the resulting fibrils show increased neurotoxicity. The mutant peptide E22Q induced apoptosis of cerebral endothelial cells at a concentration of 25 μm, whereas WT Aβ 1-40 and the Italian mutant E22K (H-6698) showed no effect.

GA20183 (Gln²²)-Amyloid β-Protein (1-42) The Dutch mutation (E22Q) aggregates more readily than the wild-type sequence. The resulting fibrils show increased neurotoxicity.

GA20184 (Gln²²,Asn²³)-Amyloid β-Protein (1-40) Transgenic mice expressing the vasculotropic Dutch/Iowa (E693Q/D694N) mutant human Aβ precursor protein in brain (Tg-SwDI) accumulate abundant cerebral microvascular fibrillar amyloid deposits and exhibit robust neuroinflammation. In vitro, the doubly mutated Aβ peptides showed an increased propensity to fibrillation and pathogenicity compared to the Dutch and Iowa single mutants.

GA20181 (Gln¹¹)-Amyloid β-Protein (1-28)

GA20186 (Gln⁹)-Amyloid β-Protein (1-40)

GA20199 (Gly²²)-Amyloid β-Protein (1-40) The highly neurotoxic arctic mutant (E22G) of Aβ has been used to study the mechanisms underlying the formation of soluble and insoluble β-amyloid aggregates. As the wild-type Aβ, the arctic mutant preferably assembles in the presence of GM1 ganglioside.

GA20200 (Gly²²)-Amyloid β-Protein (1-42) The arctic mutant of amyloid β peptide 1-42, in which Glu²² is substituted by Gly, is distinctly more amyloidogenic than the wild-type Aβ 1-42.

GA20197 (Gly²¹)-Amyloid β-Protein (1-40) Contrary to β-amyloid peptides mutated at position 22 (Dutch, Italian, Arctic mutants) the Flemish mutation (A21G) shows a decreased tendency to aggregate and a reduced neurotoxicity. In the studies of Betts and Tsubuki, A21G was degraded significantly more slowly by neprilysin than the wild-type Aβ 1-40 and the E22 mutants. The relative resistance to proteolytic degradation may account for the pathogenicity of the Aβ mutant.

GA20198 (Gly²¹)-Amyloid β-Protein (1-42) The Flemish mutation (A21G) shows a decreased tendency to aggregate and a reduced neurotoxicity. A21G is pathogenic as it is degraded significantly more slowly by neprilysin than WT Abeta42.

GA20195 (Gly¹,Ser³·²²,Gln⁴·³⁴,Thr⁶,Arg¹⁹,Tyr²¹,Ala²³·³¹,Aib³²)-Pancreatic Polypeptide (human) (Gly¹,Ser³.²²,Gln⁴.³⁴,Thr⁶,Arg¹⁹,Tyr²¹,Ala²³.³¹,Aib³²)-Pancreatic Polypeptide (human)是一种有效的选择性神经肽 Y Y5 受体激动剂，与 hY5 受体结合的 IC50 为 0.24 nM。

GA20201 (Gly²⁸,Cys³⁰)-Amyloid β-Protein (1-30) amide

GA24046 (Gly?,Thr?,Ser?)-Oxytocin

kB7-OT

The cyclopeptide kB7-OT1 was designed using the kalata B7 loop 3 as template.

GA20205 (H-Cys-Gly-OH)₂

(Cys-Gly)2, (H-Cys-Gly-OH)2, NSC 333711

NSC333711. Besides its reduced form, this product of glutathione metabolism is found in plasma.

GA20221 (Hyp³)-Bradykinin

[Hyp3]-缓激肽

(Hyp³)-缓激肽，天然存在的肽激素，是一种缓激肽受体激动剂。

GA24047 (Kyn²?)-Liraglutide trifluoroacetate salt The peptide is an impurity of Liraglutide.

GA24049 (L-Threoninol(Ac)?)-Octreotide Potential impurity of octreotide.

GA24048 (Leu¹³)-Motilin (human, porcine) (Leu¹³)-Motilin (human, porcine) has been shown to produce an excitory response in the chicken gastrointestinal tract with a different sensitivity from region to region.

GA20229 (Leu³¹,Pro³⁴)-Neuropeptide Y (human, rat) (Leu³¹,Pro³⁴)-Neuropeptide Y (human, rat) 是一种特异性的神经肽 Y Y1 受体激动剂。

GA20244 (Lys²²)-Amyloid β-Protein (1-40) The Italian mutation of β-amyloid 1-40 (E22K) aggregates more rapidly than the wild-type sequence 1-40. It showed increased neurotoxicity, which (according to a solid-phase NMR-study of Masuda et al.) may be due to the salt bridge formed between Lys²² and Asp²³ in the minor conformer. As the Arctic, Flemish, and Dutch mutants, the Italian mutant is degraded considerably more slowly than wild-type Aβ by neprilysin.

GA20245 (Lys²²)-Amyloid β-Protein (1-42) The Italian mutation (E22K) aggregates more rapidly than the wild-type sequence.

GA24050 (Lys(Ac)?)-Octreotide Potential impurity of octreotide.

GA20242 (Lys¹⁵)-Amyloid β-Protein (15-21)

Β淀粉样肽改造多肽-[LYS15]-AMYLOIDΒ-PROTEIN(15-21)

KKLVFFA contains the KLVFF sequence, which is the minimum sequence binding the full-length amyloid β-protein. It showed improved water solubility compared with KLVFF (H-3682). It can be used as a labeled probe for screening defined sequences in the full-length amyloid β-protein.

GA20251 (Met(O)³⁵)-Amyloid β-Protein (1-40) Oxidation of Met35 attenuates the formation of Aβ40 oligomers.

GA20252 (Met(O)³⁵)-Amyloid β-Protein (1-42) (Met(O)³?)-Amyloid β-protein (1-42) (H-5888), in contrast to Aβ 1-42 (H-1368), has been shown to be non-toxic to 9-11 day-old rat embryonic hippocampal neuronal cultures and not to produce any protein oxidation. It has also been demonstrated that fibril formation is not affected by Met(O)³?. For the Nle analog see H-7308.

GA20253 (Met(O)³⁵)-Amyloid β-Protein (25-35) Sulfoxide of Aβ 25-35.

GA20254 (Met(O₂)³⁵)-Amyloid β-Protein (1-42) Maiti et al. could show that, in contrast to the sulfoxide of Aβ (1-42), the sulfone was as toxic and aggregated as fast as wild-type Aβ (1-42).

GA20259 (Nle³⁵)-Amyloid β-Protein (1-40) The reactive thioether of Met³? is crucial for the activity of Aβ 1-40 and Aβ 1-42. Due to the replacement of Met by inert Nle, M35Nle Aβ 1-40 was no longer toxic to cultured hippocampal neurons and had little effect on the level of protein carbonyl residues. The Nle peptide showed the same propensity to aggregate, whereas sulfoxide formation hindered the required conformational transition from random coil to β-sheet.

GA20260 (Nle³⁵)-Amyloid β-Protein (1-42) The thioether of Met³? plays a critical role in the oxidative stress induced by Aβ 1-42 and its neurotoxicity. The norleucine analog Aβ 1-42 M35Nle forms fibrils morphologically indistinguishable from the ones of the native sequence though lacking their neurotoxicity.

GA24051 (Pro?)-Oxytocin

(Pro?)-Vasotocin

The L8P variant of oxytocin is produced by the Cebidae family of New World monkeys.

GA20283 (Pyr³)-Amyloid β-Protein (3-40) The pyroglutamate-modified amyloid-β peptides derived from Aβ40 (H-7422) and Aβ42 (H-4796) have gained considerable attention as potential key participants in the pathology of Alzheimer's disease (AD) due to their abundance in AD brain, high aggregation propensity, stability, and cellular toxicity. Aβ40 and 42 can be N-terminally truncated by action of cathepsin B. The cyclization of Glu³ is catalyzed by glutaminyl cyclase. Hence, inhibition of these enzymes could be a therapeutic approach to AD.

GA20284 (Pyr³)-Amyloid β-Protein (3-42)

(PYR3)-淀粉Β-蛋白

(Pyr³)-Amyloid β-Protein (3-42) was found to be the predominant amyloid β-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. Therefore, (Pyr³)-Aβ (3-42) is suggested to accumulate in the brain and to trigger the formation of insoluble amyloid β-peptide deposits. Nussbaum et al. studies the Prion-like behaviour and tau-dependent cytotoxicity of the truncated Aβ sequence.

GA20282 (Pyr¹¹)-Amyloid β-Protein (11-40) pEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV, the N-terminally truncated isoform of the amyloid β-protein (Aβ) beginning with a pyroglutamate (Pyr) residue at position 11 was used in experiments studying the generality of fibrillogenesis-related helix formation. Comparing the fibrillogenesis kinetics of many of the most important clinically relevant amyloid β-protein alloforms it could be observed that among these peptides (Pyr¹¹)-amyloid β-protein (11-40) exhibited the greatest retardation of fibrillization rate.