1425944-22-4

Usage

Chemical class

Organic compound
The compound contains carbon atoms and is derived from ethanamine.

Fluorenyl group

Aromatic structure
The compound has a fluorenyl group, which is a polycyclic aromatic hydrocarbon with three six-membered rings.

Nitro group

Functional group
The presence of a nitro group (-NO2) indicates the compound has an aromatic ring with an electron-withdrawing property.

Amine group

Basic functional group
The compound contains an amine group (-NH2), which can act as a base in chemical reactions and form hydrogen bonds.

Ethanamine derivative

Structural modification
2-(2-((2-nitro-9H-fluoren-9-ylidene)methyl)phenoxy)ethan-1-amine is derived from ethanamine, indicating a structural modification of the original compound.

Organic synthesis applications

Building block
The presence of the fluorenyl and nitro groups suggests that the compound may be used as a building block for more complex organic molecules.

Potential biological activity

Pharmaceutical research target
The compound's structure, with its amine group and aromatic rings, could make it an interesting target for pharmaceutical research and potential drug development.

Upstream product

• 1425944-40-6 CYD-2-10 
• 906440-37-7 2-(2-nitro-fluoren-9-ylidenemethyl)phenol 
• 607-57-8 2-nitro-9H-fluorene 
• 90-02-8 salicylaldehyde 

Relevant academic research and scientific papers

Modulation of Bax and mTOR for cancer therapeutics

A rationale exists for pharmacologic manipulation of the serine (S)184 phosphorylation site of the proapoptotic Bcl2 family member Bax as an anticancer strategy. Here, we report the refinement of the Bax agonist SMBA1 to generate CYD-2-11, which has characteristics of a suitable clinical lead compound. CYD-2-11 targeted the structural pocket proximal to S184 in the C-terminal region of Bax, directly activating its proapoptotic activity by inducing a conformational change enabling formation of Bax homooligomers in mitochondrial membranes. In murine models of small-cell and non-small cell lung cancers, including patient-derived xenograft and the genetically engineered mutant KRAS-driven lung cancer models, CYD-2-11 suppressed malignant growth without evident significant toxicity to normal tissues. In lung cancer patients treated with mTOR inhibitor RAD001, we observed enhanced S184 Bax phosphorylation in lung cancer cells and tissues that inactivates the propaoptotic function of Bax, contributing to rapalog resistance. Combined treatment of CYD-2-11 and RAD001 in murine lung cancer models displayed strong synergistic activity and overcame rapalog resistance in vitro and in vivo. Taken together, our findings provide preclinical evidence for a pharmacologic combination of Bax activation and mTOR inhibition as a rational strategy to improve lung cancer treatment.

BAX AGONIST, COMPOSITIONS, AND METHODS RELATED THERETO

The disclosure relates to BAX activators and therapeutic uses relates thereto. In certain embodiments, the disclosure relates to methods of treating or preventing cancer, such as lung cancer, comprising administering a therapeutically effective amount of a pharmaceutical composition comprising a compound disclosed herein or pharmaceutically acceptable salt to a subject in need thereof.