32082-98-7

Upstream product

• 67-56-1 methanol 
• 49551-01-1 2-anilino-4-nitrobenzoic acid 
• 100959-22-6 methyl 2-bromo-4-nitrobenzoate 
• 62-53-3 aniline 
• 16426-64-5 2-bromo-4-nitrobenzoic acid 

Downstream Products

• 118178-63-5 2-anilino-4-nitro-benzoic acid hydrazide 
• 1744-91-8 9-chloro-3-nitroacridine 
• 64894-92-4 4-(3-nitroacridin-9-ylamino)benzoic acid 
• 49551-01-1 2-anilino-4-nitrobenzoic acid 

Relevant academic research and scientific papers

MODIFIED PROTEINS AND PROTEIN DEGRADERS

Provided herein are compounds, pharmaceutical compositions, and methods for binding or degrading target proteins. Further provided herein are compounds having a DNA damage-binding protein 1 (DDB1) binding moiety. Some such embodiments include a linker. Some such embodiments include a target protein binding moiety. Further provided herein are ligand-DDB1 complexes. Further provided herein are in vivo modified DDB1 proteins.

Identification of novel 3-nitroacridines as autophagy inducers in gastric cancer cells

Dysregulated autophagy is involved in various human disorders including cancer. An autophagy-associated cell death pathway can be seen as a back-up cell death mechanism in cancer cells that are deficient in the apoptosis pathway. Therefore, many attempts have been made to induce autophagy for anticancer therapy. Anti-apoptotic Bcl-2 family proteins Bcl-2 and Bcl-xL can inhibit autophagy via binding to the BH3-only protein Beclin 1, an essential autophagy stimulator. In a previous study, we discovered several small molecule Beclin 1 mimetics as autophagy inducers through high-throughput screening and structural optimization, in which 3-nitroacridine warrants further exploration. Here, a series of novel 3-nitroacridine derivatives were designed, synthesized, and their pharmaceutical activities and mechanism of action were investigated against gastric cancer cell lines. As a result, compounds 3, 4, and 9 displayed potent cytotoxicity and induced autophagy in MGC-803 and SGC-7901 gastric cancer cells. Besides, compounds 3 and 9 also inhibited the migration of SGC-7901 cells. The development of 3-nitroacridine analogues as autophagy inducers is not only likely to be a potential strategy for cancer therapy, but it will also facilitate a better understanding of the complicated roles of autophagy in normal physiology and pathophysiology.

Monna, a potent and selective blocker for transmembrane protein with unknown function 16/anoctamin-1

Transmembrane protein with unknown function 16/anoctamin-1 (ANO1) is a protein widely expressed in mammalian tissues, and it has the properties of the classic calcium-activated chloride channel (CaCC). This protein has been implicated in numerous major physiological functions. However, the lack of effective and selective blockers has hindered a detailed study of the physiological functions of this channel. In this study, we have developed a potent and selective blocker for endogenous ANO1 in Xenopus laevis oocytes (xANO1) using a drug screening method we previously established (Oh et al., 2008). We have synthesized a number of anthranilic acid derivatives and have determined the correlation between biological activity and the nature and position of substituents in these derived compounds. A structure-activity relationship revealed novel chemical classes of xANO1 blockers. The derivatives contain a-NO2 group on position 5 of a naphthyl group-substituted anthranilic acid, and they fully blocked xANO1 chloride currents with an IC 5050 of 0.08 μM for xANO1. Selectivity tests revealed that other chloride channels such as bestrophin-1, chloride channel protein 2, and cystic fibrosis transmembrane conductance regulator were not appreciably blocked by 10～30 μM MONNA. The potent and selective blockers for ANO1 identified here should permit pharmacological dissection of ANO1/CaCC function and serve as potential candidates for drug therapy of related diseases such as hypertension, cystic fibrosis, bronchitis, asthma, and hyperalgesia.