Exendin-3
(Synonyms: 艾塞那肽) 目录号 : GC36019
Exendin-3是从吉拉怪兽蜥蜴 Heloderma horridurn 毒液分离的生物活性肽。
Cas No.:130357-25-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Kinase experiment: | Effect of increasing concentrations of two VIP receptor antagonists on the increase in amylase release are observed with VIP, secretin, or exendin-3. Male Hartley guinea pigs Acini were incubated with VIP (1 nM), secretin (1 μM), or Exendin-3 (1 μM) for 30 min at 37°C, alone or in combination with indicated concentrations of [AcTyr, D-Phe]GRF 1-29 amide (solid symbols) or [4-Cl-D-Phe,Leu] VIP (open symbols)[1]. |
References: [1]. Raufman JP, et al. Exendin-3, a novel peptide from Heloderma horridum venom, interacts with vasoactive intestinal peptide receptors and a newly described receptor on dispersed acini from guinea pig pancreas. Description of exendin-3(9-39) amide, a specific exendin receptor antagonist. J Biol Chem. 1991 Feb 15;266(5):2897-902. | |
Exendin-3 is a biologically active peptides isolated from venoms of the Gila monster lizards, Heloderma horridurn . VIP receptor, putative exendin receptor[1]
Exendin-3 interacts with at least two receptors on guinea pig pancreatic acini; at high concentrations (>100 nM) the peptide interacts with VIP receptors, thereby causing a large increase in cAMP and stimulating amylase release; at lower concentrations (0.1-3 nM) the peptide interacts with a putative exendin receptor, thereby causing a smaller increase in cAMP of undetermined function[1].
[1]. Raufman JP, et al. Exendin-3, a novel peptide from Heloderma horridum venom, interacts with vasoactive intestinal peptide receptors and a newly described receptor on dispersed acini from guinea pig pancreas. Description of exendin-3(9-39) amide, a specific exendin receptor antagonist. J Biol Chem. 1991 Feb 15;266(5):2897-902.
| Cas No. | 130357-25-4 | SDF | |
| 别名 | 艾塞那肽 | ||
| 分子式 | C184H282N50O61S | 分子量 | 4202.57 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.2379 mL | 1.1897 mL | 2.3795 mL |
| 5 mM | 0.0476 mL | 0.2379 mL | 0.4759 mL |
| 10 mM | 0.0238 mL | 0.119 mL | 0.2379 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Exendin peptides
Mt Sinai J Med 1992 Mar;59(2):147-9.PMID:1574068doi
Exendin-3 and exendin-4 are biologically active peptides isolated from venoms of the Gila monster lizards, H. horridum and H. suspectum, respectively. They were isolated using a chemical assay which detects peptides with amino-terminal histidine residues. Both are 39 amino acid peptides containing an amino-terminal histidine and a carboxyl-terminal serine amide and are members of the glucagon superfamily of peptide hormones. When tested in a dispersed pancreatic acinar cell assay, Exendin-3 stimulates amylase release and with increasing concentrations causes a biphasic increase in cellular cAMP. In contrast, exendin-4 at concentrations up to 1 microM does not stimulate amylase release and produces a monophasic increase in cellular cAMP despite differing from Exendin-3 by only two amino acid substitutions at positions 2 and 3 from the N-terminus. Endogenous Mammalian Analog to Exendins? The differences in biological activities can be explained by the observation that Exendin-3 interacts with VIP receptors to stimulate amylase release, whereas exendin-4 does not. Both Exendin-3 and exendin-4 interact with a putative exendin receptor on pancreatic acinar cells. The presence of this receptor was determined and defined by the ability of a specific inhibitor, exendin(9-39) amide, to abolish the increase in cAMP observed with 0.1-3 nM Exendin-3 or exendin-4. The presence of the exendin receptor, although functionally undefined at the present time, predicts the existence of an endogenous mammalian analog to the exendin peptides.
68Ga-labelled Exendin-3, a new agent for the detection of insulinomas with PET
Eur J Nucl Med Mol Imaging 2010 Jul;37(7):1345-55.PMID:20111963DOI:10.1007/s00259-009-1363-y.
Purpose: Insulinomas are neuroendocrine tumours derived from pancreatic beta-cells. The glucagon-like peptide 1 receptor (GLP-1R) is expressed with a high incidence (>90%) and high density in insulinomas. Glucagon-like peptide 1 (GLP-1), the natural ligand of GLP-1R, is rapidly degraded in vivo. A more stable agonist of GLP-1R is Exendin-3. We investigated imaging of insulinomas with DOTA-conjugated Exendin-3 labelled with (68)Ga. Methods: Targeting of insulinomas with [Lys(40)(DOTA)]Exendin-3 labelled with either (111)In or (68)Ga was investigated in vitro using insulinoma tumour cells (INS-1). [Lys(40)((111)In-DTPA)]Exendin-3 was used as a reference in this study. In vivo targeting was investigated in BALB/c nude mice with subcutaneous INS-1 tumours. PET imaging was performed using a preclinical PET/CT scanner. Results: In vitro Exendin-3 specifically bound and was internalized by GLP-1R-positive cells. In BALB/c nude mice with subcutaneous INS-1 tumours a high uptake of [Lys(40)((111)In-DTPA)]Exendin-3 in the tumour was observed (33.5 +/- 11.6%ID/g at 4 h after injection). Uptake was specific, as determined by coinjection of an excess of unlabelled [Lys(40)]Exendin-3 (1.8 +/- 0.1%ID/g). The pancreas also exhibited high and specific uptake (11.3 +/- 1.0%ID/g). High uptake was also found in the kidneys (144 +/- 24%ID/g) and this uptake was not receptor-mediated. In this murine tumour model optimal targeting of the GLP-1R expressing tumour was obtained at exendin doses < or =0.1 microg. Remarkably, tumour uptake of (68)Ga-labelled [Lys(40)(DOTA)]Exendin-3 was lower (8.9 +/- 3.1%ID/g) than tumour uptake of (111)In-labelled [Lys(40)(DTPA)]Exendin-3 (25.4 +/- 7.2%ID/g). The subcutaneous tumours were clearly visualized by small-animal PET imaging after injection of 3 MBq of [Lys(40)((68)Ga-DOTA)]Exendin-3. Conclusion: [Lys(40)((68)Ga-DOTA)]Exendin-3 specifically accumulates in insulinomas, although the uptake is lower than that of [Lys(40)((111)In-DTPA)]Exendin-3. Therefore, [Lys(40)((68)Ga-DOTA)]Exendin-3 is a promising tracer to visualize insulinomas with PET.
Noninvasive Imaging of Islet Transplants with 111In-Exendin-3 SPECT/CT
J Nucl Med 2016 May;57(5):799-804.PMID:26795287DOI:10.2967/jnumed.115.166330.
Islet transplantation is a promising treatment for type 1 diabetic patients. However, there is acute as well as chronic loss of islets after transplantation. A noninvasive imaging method that could monitor islet mass might help to improve transplantation outcomes. In this study, islets were visualized after transplantation in a rat model with a dedicated small-animal SPECT scanner by targeting the glucagonlike peptide-1 receptor (GLP-1R), specifically expressed on β-cells, with (111)In-labeled Exendin-3. Methods: Targeting of (111)In-exendin-3 to GLP-1R was tested in vitro on isolated islets of WAG/Rij rats. For in vivo evaluation, 400 or 800 islets were transplanted into the calf muscle of WAG/Rij rats (6-8 wk old). Four weeks after transplantation, SPECT/CT images were acquired 1 h after injection of (111)In-labeled Exendin-3. After SPECT acquisition, the muscles containing the transplant were analyzed immunohistochemically and autoradiographically. Results: The binding assay, performed on isolated islets, showed a linear correlation between the number of islets and (111)In-exendin-3 accumulation (Pearson r = 0.98). In vivo, a 1.70 ± 0.44-fold difference in tracer uptake between 400 and 800 transplanted islets was observed. Ex vivo analysis of the islet transplant showed colocalization of tracer accumulation on autoradiography, with insulin-positive cells and GLP-1R expression on immunohistochemistry. Conclusion: (111)In-exendin-3 accumulates specifically in the β-cells after islet transplantation and is a promising tracer for noninvasive monitoring of the islet mass.
Exendin-3, a novel peptide from Heloderma horridum venom, interacts with vasoactive intestinal peptide receptors and a newly described receptor on dispersed acini from guinea pig pancreas. Description of Exendin-3(9-39) amide, a specific exendin receptor antagonist
J Biol Chem 1991 Feb 15;266(5):2897-902.PMID:1704369doi
Exendin-3 increased cellular cAMP levels and amylase release from dispersed acini from guinea pig pancreas. Low concentrations (0.1-3 nM) caused a 12-fold increase in cAMP, whereas higher concentrations (0.3-3 microM) caused an additional 24-fold increase in cAMP. Maximal cAMP with the highest concentration tested was the same as the maximal response with secretin, vasoactive intestinal peptide (VIP), peptide histidine isoleucine, helodermin, or helospectin-I. In terms of amylase release, Exendin-3 had the same efficacy but was the least potent of these peptides. Exendin-3-induced increases in amylase release were inhibited by VIP receptor antagonists and the new peptide (greater than 0.1 microM) competed with radiolabeled VIP for binding sites on dispersed acini. Increasing concentrations of an Exendin-3 fragment, Exendin-3(9-39) amide, did not increase cAMP or amylase release but inhibited the increase in cAMP observed with 0.1-3 nM Exendin-3. The fragment did not alter the effects of other peptides that are known to increase acinar cAMP. We conclude that Exendin-3 interacts with at least two receptors on guinea pig pancreatic acini; at high concentrations (greater than 100 nM) the peptide interacts with VIP receptors, thereby causing a large increase in cAMP and stimulating amylase release; at lower concentrations (0.1-3 nM) the peptide interacts with a putative exendin receptor, thereby causing a smaller increase in cAMP of undetermined function. Exendin-3(9-39) amide is a specific exendin receptor antagonist.
Isolation and characterization of exendin-4, an Exendin-3 analogue, from Heloderma suspectum venom. Further evidence for an exendin receptor on dispersed acini from guinea pig pancreas
J Biol Chem 1992 Apr 15;267(11):7402-5.PMID:1313797doi
The recent identification in Heloderma horridum venom of Exendin-3, a new member of the glucagon superfamily that acts as a pancreatic secretagogue, prompted a search for a similar peptide in Heloderma suspectum venom. An amino acid sequencing assay for peptides containing an amino-terminal histidine residue (His1) was used to isolate a 39-amino acid peptide, exendin-4, from H. suspectum venom. Exendin-4 differs from Exendin-3 by two amino acid substitutions, Gly2-Glu3 in place of Ser2-Asp3, but is otherwise identical. The structural differences make exendin-4 distinct from Exendin-3 in its bioactivity. In dispersed acini from guinea pig pancreas, natural and synthetic exendin-4 stimulate a monophasic increase in cAMP beginning at 100 pM that plateaus at 10 nM. The exendin-4-induced increase in cAMP is inhibited progressively by increasing concentrations of the exendin receptor antagonist, exendin-(9-39) amide. Unlike Exendin-3, exendin-4 does not stimulate a second rise in acinar cAMP at concentrations greater than 100 nM, does not stimulate amylase release, and does not inhibit the binding of radiolabeled vasoactive intestinal peptide to acini. This indicates that in dispersed pancreatic acini, exendin-4 interacts only with the recently described exendin receptor.