INY-03-041 trihydrochloride

 Cat No.: BP-400172 4.5  

INY-03-041 trihydrochloride is the trihydrochloride salt form of INY-03-041, a cereblon-recruiting pan-AKT PROTAC degrader. Public sources describe the compound as consisting of the ATP-competitive AKT inhibitor ipatasertib conjugated to lenalidomide, which functions as the cereblon ligand. The AKT-recognition module engages the kinase domain of AKT isoforms, while the lenalidomide-derived portion recruits CRL4-cereblon; the linker enables productive ternary-complex formation. Mechanistically, INY-03-041 trihydrochloride induces degradation of AKT family proteins through ubiquitination and proteasome-dependent removal, enabling pathway suppression beyond kinase occupancy. It is useful for studying PI3K–AKT signaling, AKT isoform dependence, feedback pathway adaptation, cereblon-based kinase degrader design, and comparisons between AKT catalytic inhibition and AKT protein depletion in cancer-relevant cellular models.

INY-03-041 trihydrochloride

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Category
PROTAC
Molecular Formula
C44H59Cl4N7O5
Molecular Weight
907.8
Appearance
Solid

* For research and manufacturing use only. Not for human or clinical use.

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Appearance
Solid
Storage
Store at -20°C
Mechanism

INY-03-041 trihydrochloride

Target: INY-03-041 trihydrochloride targets AKT1, AKT2, and AKT3 kinase isoforms.

Binding site: Its ipatasertib warhead binds the ATP-competitive catalytic pocket of AKT kinases.

Mechanism of action: INY-03-041 trihydrochloride is the trihydrochloride salt form of a selective pan-AKT PROTAC degrader. It combines the ATP-competitive AKT inhibitor ipatasertib with the cereblon ligand lenalidomide, enabling recruitment of AKT1, AKT2, and AKT3 to CRL4CRBN ubiquitin ligase machinery. This proximity-driven mechanism promotes AKT ubiquitination and proteasome-mediated degradation, producing sustained suppression of downstream AKT signaling beyond reversible kinase inhibition. The compound is useful for studying AKT isoform dependency, pathway durability, degradation kinetics, and concentration-dependent degradation behavior in PI3K/AKT pathway models.

Applications

• PROTAC-Mediated Kinase Degradation: INY-03-041 trihydrochloride is utilized in research to selectively degrade kinase proteins, enabling the study of kinase signaling pathways. This aids in understanding the role of specific kinases in cellular processes and disease mechanisms, providing insights into potential therapeutic targets.

• Targeted Protein Degradation in Oncology: Researchers apply INY-03-041 trihydrochloride to investigate the degradation of oncogenic proteins. This application is crucial for exploring novel cancer treatment strategies by eliminating proteins that drive tumor growth and survival.

• Investigating Protein-Protein Interactions: By facilitating the targeted degradation of specific proteins, INY-03-041 trihydrochloride helps elucidate protein-protein interactions within cells. This application is vital for mapping interaction networks and understanding the functional consequences of disrupting these interactions.

• PROTAC-Induced Protein Knockdown: INY-03-041 trihydrochloride enables researchers to achieve precise protein knockdown, offering a powerful tool for studying protein function and validating drug targets. This approach is essential for dissecting complex biological pathways and identifying potential intervention points.

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L

* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2

* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O c22h30n40
g/mol
g

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