TRV-120027 TFA

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TRV-120027 TFA
Details
CAS: No unified CAS for salt form (free peptide is an AT₁R biased ligand)
Core structure: β-arrestin-biased agonist of angiotensin II type 1 receptor (AT₁R), a functional peptide site-specifically modified based on the angiotensin II backbone. It selectively activates the β-arrestin signaling pathway downstream of AT₁R without activating the classic G protein-dependent vasoconstrictive and hypertensive pathways, achieving targeted cardiovascular protective effects.
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**Related documents**
COA/MS/HPLC Report
Peptide Dissolution and Storage Guide
Category
Pharmaceutical Peptides
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Description

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Product Name TRV-120027 TFA
Description TRV-120027 is a classic β-arrestin-biased agonist of the AT₁ receptor. It specifically binds to the AT₁ receptor and induces a specific conformational change, selectively activating the downstream β-arrestin-mediated signaling pathway to promote cardiomyocyte survival, inhibit apoptosis and ameliorate cardiac remodeling, without activating traditional G protein-dependent effects such as vasoconstriction and blood pressure elevation. It exhibits definite cardioprotective and cardiac function-improving effects in models of heart failure, myocardial ischemia-reperfusion injury and cardiac hypertrophy, without obvious hypertensive side effects. It is a core tool peptide for studying biased signal transduction of G protein-coupled receptors and cardiovascular protection mechanisms, and is also widely used in the development of novel biased cardiovascular drugs.
Peptide Purity (HPLC, %) 95% / 98% / 99%
Free base molecular formula C₅₁H₇₃N₁₃O₁₂
Free base molecular weight (Da) 1060.2, higher for TFA salt form
Structure type Modified octapeptide with β-arrestin-biased design, trifluoroacetate salt

 

Product Basic Information Table

 

Product Standard English Name Product Abbreviation / Alias Function Tags (comma-separated) Core Structure Molecular Formula Exact Mass (Da) Average MW (Da) Salt Form Length (aa)
TRV-120027 TFA TRV-120027 trifluoroacetate AT₁ receptor β-arrestin-biased agonist, cardioprotection, GPCR biased signaling research Functional octapeptide site-modified from angiotensin II backbone; selectively activates β-arrestin pathway downstream of AT₁R without activating G protein-dependent vasoconstrictive pathway C₅₁H₇₃N₁₃O₁₂ 1059.55 1060.2 Trifluoroacetate (TFA) 8

Physicochemical Solubility & Storage Parameters

 

Product Code Appearance Long-term Storage Short-term Storage Solution Stability Solid Powder Stability
PEP-TRV001 white powder Store at -20°C, sealed, dry and protected from light. Aliquot to avoid repeated freeze-thaw cycles. Stable for 1 month at 2–8°C in sealed dry condition; ship on ice pack recommended. Stable for 7 days at 4°C. Moderate water solubility, assisted by dilute acetic acid or acidic buffer; freely soluble in DMSO. Aqueous solution is susceptible to peptidase degradation; prepare fresh before use. Stable for 3 years at -20°C, dry and protected from light.

Functional Description

 

Product Code Frontend Short Summary (for search list display) Detailed Biological Function Description Applicable Research Areas (comma-separated) Targets / Pathways
PEP-TRV001 AT₁ receptor β-arrestin-biased agonist with targeted cardioprotection and no hypertensive side effect TRV-120027 is a classic β-arrestin-biased agonist of the angiotensin II type 1 receptor (AT₁R). It specifically binds to the AT₁ receptor and induces a specific conformational change, selectively activating the downstream β-arrestin-mediated signaling pathway to promote cardiomyocyte survival, inhibit apoptosis, ameliorate cardiac remodeling and reduce myocardial fibrosis. Meanwhile, it does not activate traditional G protein-dependent effects such as vasoconstriction and blood pressure elevation, avoiding the hypertensive side effects of conventional AT₁ agonists. It exhibits definite cardioprotective and cardiac function-improving effects in models of heart failure, myocardial ischemia-reperfusion injury and cardiac hypertrophy. It is a core tool peptide for studying biased signal transduction of G protein-coupled receptors and cardiovascular protection mechanisms, and is also widely used in the development of novel biased cardiovascular drugs. GPCR biased signaling research, heart failure mechanism study, myocardial ischemia-reperfusion injury research, cardiac remodeling & fibrosis study, cardiovascular drug development Angiotensin II type 1 receptor (AT₁R); β-arrestin signaling pathway; Cardiomyocyte survival pathway

 

 

 

 

 

 

 

 

 

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