| Size | Price | Stock | Qty |
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| 100mg |
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| 250mg |
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| 500mg |
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| 1g |
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| Other Sizes |
| Targets |
Insulin secretion
Glucagon (19-29) targets the pancreatic beta cells to inhibit insulin secretion. Its mechanism involves the hyperpolarization of voltage-dependent Ca²⁺ channels through a pathway linked to a pertussis toxin-sensitive G protein. It also acts as a potent Ca²⁺/Mg²⁺-ATPase inhibitor. The peptide exerts a potent negative inotropic action in cardiac tissues and stimulates glycogenolysis and gluconeogenesis in the liver. |
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| ln Vitro |
Glucagon (19–29) has a strong negative inotropic effect at concentrations between 0.1 pM and 1 nM. The combination of 30 nM glucagon and 1 nM glucagon (19–29)[3] results in a 45% increase in the amplitude of cell contractility, which is the most notable observation.
Glucagon (19-29), from 0.1 pM to 1 nM, exerts a potent negative inotropic action. It dose-dependently inhibits insulin secretion induced by 8.3 M glucose. A concentration of 1 nM significantly inhibits glucagon-like peptide 1 (7-36) amide-potentiated insulin secretion. It is a potent and efficient inhibitor of insulin release. |
| ln Vivo |
Glucagon (19-29) is the COOH-terminal (19-29) fragment that is extracted from glucagon. It is also referred to as Miniglucagon. Insulin secretion induced by 8.3 M glucose is dose-dependently inhibited by glucagon (19–29), while the perfusion flow rate remains unchanged. A 1 nM glucagon-like peptide 1 (7-36) amide-potentiated insulin secretion is significantly inhibited by a concentration of 1 nM glucagon (19-29)[1]. By hyperpolarizing voltage-dependent Ca2+ channels connected to a pathway involving a pertussis toxin-sensitive G protein, glucagon (19–29) is a highly effective and potent inhibitor of insulin release[2].
In rat studies, miniglucagon (Glucagon (19-29)) at concentrations of 1, 10, 100, and 1,000 pM was perfused to assess its impact on stimulated insulin secretion. The peptide inhibits insulin secretion in a dose-dependent manner. Its ability to hyperpolarize Ca²⁺ channels via a pertussis toxin-sensitive G protein has been demonstrated in these models. |
| Enzyme Assay |
In vitro enzyme assays for Glucagon (19-29) can measure its inhibition of Ca²⁺/Mg²⁺-ATPase activity. The enzyme is incubated with the peptide and ATP, and the release of inorganic phosphate is quantified. Receptor binding studies can assess its interaction with the glucagon receptor or other target proteins. Its effects on insulin secretion can be studied using isolated pancreatic islets.
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| Cell Assay |
In vitro cellular assays for Glucagon (19-29) involve treating pancreatic beta cells with the peptide to measure its inhibition of insulin secretion. Insulin released into the culture medium is quantified by ELISA or radioimmunoassay. Its negative inotropic effects can be studied in isolated cardiac myocytes by measuring cell contractility.
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| Animal Protocol |
Rats: Miniglucagon (1, 10, 100, and 1,000 pM) is perfused with or without 1 nM tGLP-1 during the 45-minute equilibration period, in order to assess the impact of miniglucagon (Glucagon (19-29)) on stimulated insulin secretion. To study the glucagon and miniglucagon secretion, the glucose concentration is switched from 11 to 3 mM after a 45-min stabilization period, and the peptides secreted are measured by radioimmunoassay[1].
In vivo animal models for Glucagon (19-29) include rat perfusion studies to assess its effects on insulin secretion. In these studies, the pancreas is perfused with the peptide, and insulin levels in the perfusate are measured. The peptide's effects on glucose metabolism can be studied in vivo by measuring blood glucose levels after administration. |
| ADME/Pharmacokinetics |
Pharmacokinetic data for Glucagon (19-29) are limited. As a peptide, it is likely to have a short half-life due to rapid degradation by peptidases. It is typically administered by injection in research settings. Its distribution and metabolism are not well-characterized, but it is expected to be cleared rapidly from the circulation.
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| Toxicity/Toxicokinetics |
The toxicological profile of Glucagon (19-29) is not extensively documented. As an endogenous peptide, it is part of the body's normal physiology. However, its pharmacological effects, particularly the inhibition of insulin secretion, could lead to hyperglycemia if administered in excess. Its safety in humans has not been established for therapeutic use.
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| References |
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| Additional Infomation |
Glucagon (19-29) is an endogenous short peptide known as Miniglucagon, derived from the C-terminal portion of glucagon. It is a potent inhibitor of insulin secretion, acting through a pertussis toxin-sensitive G protein pathway to hyperpolarize Ca²⁺ channels. It also has negative inotropic effects and stimulates glycogenolysis and gluconeogenesis.
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| Molecular Formula |
C61H89N15O18S
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|---|---|
| Molecular Weight |
1352.53
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| Exact Mass |
1351.62
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| Elemental Analysis |
C 54.17; H, 6.63; N, 15.53; O, 21.29; S, 2.37
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| CAS # |
64790-15-4
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| Related CAS # |
64790-15-4
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| PubChem CID |
3080901
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| Appearance |
Solid powder
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| Density |
1.339 g/cm3
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| Boiling Point |
1828.5ºC at 760 mmHg
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| Flash Point |
1059.6ºC
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| Index of Refraction |
1.596
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| LogP |
2.66
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| Hydrogen Bond Donor Count |
18
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| Hydrogen Bond Acceptor Count |
20
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| Rotatable Bond Count |
42
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| Heavy Atom Count |
95
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| Complexity |
2700
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| Defined Atom Stereocenter Count |
12
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| SMILES |
CC(C[C@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](N)C)=O)CCC(N)=O)=O)CC(O)=O)=O)CC1=CC=CC=C1)=O)C(C)C)=O)CCC(N)=O)=O)CC2=CNC3=CC=CC=C23)=O)C(N[C@H](C(N[C@H](C(N[C@H](C(O)=O)[C@H](O)C)=O)CC(N)=O)=O)CCSC)=O)C
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| InChi Key |
SVHJFTNFNMWDBS-FPLSMPAJSA-N
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| InChi Code |
InChI=1S/C61H89N15O18S/c1-29(2)23-40(55(87)68-39(21-22-95-7)54(86)73-43(26-47(65)80)59(91)76-50(32(6)77)61(93)94)70-56(88)42(25-34-28-66-36-16-12-11-15-35(34)36)72-53(85)38(18-20-46(64)79)69-60(92)49(30(3)4)75-58(90)41(24-33-13-9-8-10-14-33)71-57(89)44(27-48(81)82)74-52(84)37(17-19-45(63)78)67-51(83)31(5)62/h8-16,28-32,37-44,49-50,66,77H,17-27,62H2,1-7H3,(H2,63,78)(H2,64,79)(H2,65,80)(H,67,83)(H,68,87)(H,69,92)(H,70,88)(H,71,89)(H,72,85)(H,73,86)(H,74,84)(H,75,90)(H,76,91)(H,81,82)(H,93,94)/t31-,32+,37-,38-,39-,40-,41-,42-,43-,44-,49-,50-/m0/s1
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| Chemical Name |
(3S)-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-3-[[(2S)-5-amino-2-[[(2S)-2-aminopropanoyl]amino]-5-oxopentanoyl]amino]-4-oxobutanoic acid
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| Synonyms |
Miniglucagon; Des(1-18) glucagon; Glucagon (19-29)
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| HS Tariff Code |
2934.99.03.00
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: ≥ 25 mg/mL (~18.5 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (1.85 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (1.85 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (1.85 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.7394 mL | 3.6968 mL | 7.3936 mL | |
| 5 mM | 0.1479 mL | 0.7394 mL | 1.4787 mL | |
| 10 mM | 0.0739 mL | 0.3697 mL | 0.7394 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.