Survodutide TFA
Based on 1 Customer Validation
Survodutide (BI 456906) TFA is a potent, selective glucagon receptor/GLP-1 receptor (GCGR/GLP-1R) dual agonist with EC50s of 0.52 nM and 0.33 nM in CHO-K1 cells, respectively. Survodutide TFA, a 29-amino-acid peptide, is a potent acylated peptide containing a C18 fatty acid. Survodutide TFA has robust anti-obesity efficacy achieved by increasing energy expenditure and decreasing food intake.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 99.39%
- 分子式: C192H289N47O61·xC2HF3OC2
- 分子量:4231.62 (free base)
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保管条件:
Sealed storage, away from moisture and light.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
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溶剤 & 溶解度
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
体外実験
The EC50 is 0.36 nM for Survodutide (BI 456906) TFA in the endogenous mouse GLP-1R in the insulinoma cell line MIN6, and the EC50 is 60 pM for GLP-1. In 0.5% human and mouse plasma, Survodutide TFA shows a similar potency to that of endogenous GLP-1. For the GCGR, in 0.5% human and mouse plasma, Survodutide TFA is 6-fold less potent (0.29 and 0.17 nM, respectively) in relation to endogenous glucagon (47 and 30 pM, respectively)[1].
Proteolytic stability of Survodutide TFA is helped by C-terminal amidation and the introduction of a non-coded amino acid 1-aminocyclobutane-1-carboxylic acid (Ac4c) in position 2, well established as the site of proteolytic activity for dipeptidyl peptidase-4. The desired extended terminal half-life of Survodutide TFA is achieved by the introduction of a glycine-serine linker in position 24, carrying a C18 di-acid[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
体内実験
Survodutide (1, 3, 10, 30, 100 nmol/kg; SC; single dose) TFA dose-dependently reducesacute food intake in WT but not in GLP-1R KO mice (Three-week-old, male, lean NMRI outbred mice)[1].
Survodutide (1, 3, 10, 30, 100 nmol/kg; SC; single dose) TFA engages the glucagon receptor in vivo upon single dosing, increases liver nicotinamide N-methyltransferase mRNA, and reduces plasma serine and glutamine[1].
Survodutide (SC injection) TFA causes mean residence times of 44 and 140 h and Tmax values of 7 and 51 h obtained in mice and dogs, respectively[1].
Pharmacokinetic Parameters of Survodutide (BI 456906) in mice and dogs[1].
| Mice (20 nmol/kg; SC) | Dogs (10 nmol/kg; SC) | |
| Tmax (h) | 7 | 50.7 |
| Cmax (nM) | 84.9 | 62.0 |
| AUC0-∞ (nM h) | 4640 | 9540 |
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male C57BL6/J mice pre-fed with a 60% HFD (22 weeks)[1]
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Dosage:3, 10, 20, 30 nmol/kg
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Administration:SC; daily; 30 days
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Result:Dose-dependently reduced bodyweight from baseline by up to 32% at Day 28 at a dose of 30 nmol/kg.
臨床実験
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
化学情報
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性状 Solid
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分子量 4231.62 (free base)
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分子式 C192H289N47O61·xC2HF3OC2
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Color White to off-white
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別名
BI 456906 TFA
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配列
His-{1-Aminocyclobutanecarboxylic acid}-Gln-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Lys-Tyr-Leu-Asp-Glu-Arg-Ala-Ala-Lys-Asp-Phe-Ile-{Lys(Gly-Gly-Ser-Gly-Ser-Gly-γGlu-C18 diacid)}-Trp-Leu-Glu-Ser-Ala-NH2
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シーケンスの短縮
H-{1-Aminocyclobutanecarboxylic acid}-QGTFTSDYSKYLDERAAKDFI-{Lys(GGSGSG-γGlu-C18 diacid)}-WLESA-NH2
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Sealed storage, away from moisture and light
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
溶剤 & 溶解度
体外:
DMSO : ≥ 100 mg/mL
H2O : ≥ 100 mg/mL
* "≥" means soluble, but saturation unknown.
プロトコル
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
純度とドキュメンテーション
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データシート (295 KB)
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SDS (252 KB)
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- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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取扱説明書 (2659 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
Survodutide TFA 関連分類
HY-P4146A 関連分類
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