Tezusomant
Tezusomant is a growth hormone receptor antagonist. Tezusomant is promising for research on diseases caused by excessive growth hormone secretion, such as acromegaly.
For research use only. We do not sell to patients.
- CAS No.: 2802416-72-2
- Formula: C120H171N23O32S
- Molecular Weight:2479.84
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Tezusomant is a growth hormone receptor antagonist that effectively inhibits the activity of growth hormone and facilitates the research of various disorders caused by excessive growth hormone secretion[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2802416-72-2
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Molecular Weight 2479.84
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Formula C120H171N23O32S
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Sequence
{N-sulfanylacetyl-Phe(p-COOH)}-{Lys(Me)}-Val-Val-Ser-Asn-{Trp(CH2CO)}-{Phe(p-COOH)}-Lys-{Trp(OH)}-{Aib}-Val-Ala-{Lys(NH2)}-gGlu-{gGlu(C16 diacid)} (covalent bridge:Lys2-Trp7; sulfide bridge:Phe1-Ala13)
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Sequence Shortening
{N-sulfanylacetyl-Phe(p-COOH)}-{Lys(Me)}-VVSNW-{Trp(CH2CO)}-{Phe(p-COOH)}-K-{Trp(OH)}-{Aib}-VA-{Lys(NH2)}-gGlu-{gGlu(C16 diacid)} (covalent bridge:Lys2-Trp7; sulfide bridge:Phe1-Ala13)
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Tezusomant Related Classifications
HY-P10964 Related Classifications
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