pTH-Related Protein (7-34) amide (human, mouse, rat) acetate
Based on 1 Customer Validation
pTH-Related Protein (7-34) amide (human, mouse, rat) acetate is a potent antagonist of parathyroid hormone (PTH).
For research use only. We do not sell to patients.
- Formula: C153H247N49O37·xC2HF3O2
- Molecular Weight:3364.90 (free base)
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Biological Activity
Description
Chemical Information
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Appearance Solid
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Molecular Weight 3364.90 (free base)
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Formula C153H247N49O37·xC2HF3O2
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SMILES
O=C(N[C@@H](CC(C)C)C(N[C@@H](CC1=CNC=N1)C(N[C@@H](CC(O)=O)C(N[C@@H](CCCCN)C(NCC(N[C@@H](CCCCN)C(N[C@@H](CO)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCC(N)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC2=CC=CC=C2)C(N[C@@H](CC3=CC=CC=C3)C(N[C@@H](CC(C)C)C(N[C@@H](CC4=CNC=N4)C(N[C@@H](CC5=CNC=N5)C(N[C@@H](CC(C)C)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](C)C(N[C@@H](CCC(O)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CC6=CNC=N6)C(N[C@@H]([C@H](O)C)C(N[C@@H](C)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CC(C)C)N.CC(O)=O.[x]
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Sequence
Leu-Leu-His-Asp-Lys-Gly-Lys-Ser-Ile-Gln-Asp-Leu-Arg-Arg-Arg-Phe-Phe-Leu-His-His-Leu-Ile-Ala-Glu-Ile-His-Thr-Ala-NH2
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Sequence Shortening
LLHDKGKSIQDLRRRFFLHHLIAEIHTA-NH2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
In Vitro:
DMSO : 50 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Protocols
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Purity & Documentation
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)