959150-64-2

Basic information

• Product Name: (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione
• Synonyms: (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione
• CAS NO: 959150-64-2
• Molecular Weight: 384.13
• Mol File: 959150-64-2.mol
• Article Data: 7

Chemical Properties

• CAS DataBase Reference: (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione(CAS DataBase Reference)
• NIST Chemistry Reference: (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione(959150-64-2)
• EPA Substance Registry System: (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione(959150-64-2)

Safety Data

• Hazardous Substances Data: 959150-64-2(Hazardous Substances Data)

Usage

Description

(RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione is a chemical compound that belongs to the class of isoindole-1,3-dione derivatives. It is characterized by the presence of a piperidin-3-yl group, a 4-iodoisoindole-1,3-dione core, and a ketone group. (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione holds potential pharmacological significance and may be utilized in the development of pharmaceuticals or serve as a reference standard in chemical analysis. It is crucial to handle this compound with care and follow safety protocols when working with it in a laboratory environment.

Uses

Used in Pharmaceutical Development:
(RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione is used as a compound in the pharmaceutical industry for the development of new drugs. Its unique structure and potential pharmacological properties make it a promising candidate for creating novel therapeutic agents.
Used in Chemical Analysis:
In the field of chemical analysis, (RS)-2-(2,6-dioxopiperidin-3-yl)-4-iodoisoindole-1,3-dione is used as a reference standard. Its distinct characteristics allow it to be employed as a benchmark for comparison and calibration in various analytical techniques, ensuring accurate and reliable results.

Upstream product

• 28418-88-4 3-iodophthalic anhydride 
• 24666-56-6 rac-α-aminoglutarimide hydrochloride 
• 2353-44-8 (+/-)-α-aminoglutarimide 
• 590365-46-1 (RS)-2,6-dioxopiperidin-3-yl-ammonium trifluoroacetate 

Downstream Products

• 927671-11-2 2-(2,6-dioxopiperidin-3-yl)-4-{[4-(dimethylamino)phenyl]amino}isoindole-1,3-dione 
• 927671-03-2 2-(2,6-DIOXOPIPERIDIN-3-YL)-4-(4-METHOXYPHENYLAMINO)-ISOINDOLE-1,3-DIONE 
• 927670-99-3 4-(4-tert-butylphenylamino)-2-(2,6-dioxopiperidin-3-yl)isoindole-1,3-dione 
• 927671-00-9 4-(4-isopropylphenylamino)-2-(2,6-dioxopiperidin-3-yl)isoindole-1,3-dione 
• 1216805-36-5 (RS)-2-(2,6-dioxopiperidin-3-yl)-4-phenylisoindole-1,3-dione 
• 1216805-37-6 (RS)-2-(2,6-dioxopiperidin-3-yl)-4-p-tolylisoindole-1,3-dione 
• 1216805-39-8 (RS)-2-(2,6-dioxopiperidin-3-yl)-4-(4-isobutylphenyl)isoindoline-1,3-dione 
• 1216805-45-6 (RS)-2-(2,6-dioxopiperidin-3-yl)-4-(4-isopropoxyphenyl)-isoindoline-1,3-dione 
• 1216805-41-2 (RS)-2-(2,6-dioxopiperidin-3-yl)-4-(4-hydroxyphenyl)isoindoline-1,3-dione 

Relevant articles and documents

Proteolysis-Targeting Chimera (PROTAC) Modification of Dovitinib Enhances the Antiproliferative Effect against FLT3-ITD-Positive Acute Myeloid Leukemia Cells

Acute myeloid leukemia (AML) refers to one of the most lethal blood malignancies worldwide. FLT3-ITD mutation is recognized as the most common one that predicted a poorer prognosis. There have been many prominent FLT3-ITD inhibitors approved by the FDA for clinical therapies. However, as impacted by undesirable off-target effects, differentiated metabolic issues, and clinical drug resistance problems, it remains challenging to discover alternative and promising solutions for treating FLT3-ITD+ AML. In this study, dovitinib was chemically modified and converted into CRBN-recruiting PROTACs. Two active compounds were identified, which showed enhanced antiproliferative effects against FLT3-ITD+ AML cells, both in vitro and in vivo. As demonstrated from further biological evaluation, the compounds could induce the degradation of the FLT3-ITD and KIT proteins in a ubiquitin-proteasome-dependent manner and completely block their downstream signaling pathway. The findings of this study would provide another promising strategy to develop novel therapies for FLT3-ITD+ AML.

In vitro and in vivo degradation of programmed cell death ligand 1 (PD-L1) by a proteolysis targeting chimera (PROTAC)

Immunotherapy via immune checkpoints blockade has aroused the attention of researchers worldwide. Inhibition of the programmed cell death-1 (PD-1)/programmed cell death-ligand 1 (PD-L1) interaction has been one of the most promising immunotherapy strategies. Several neutralizing antibodies targeting this interaction have been developed, which have already achieved considerable clinical success. Additionally, numerous pharmaceutical companies have been committed to develop small molecules which could block the interaction between PD-1 and PD-L1. In this study, a novel PROTAC molecule 21a was developed, and effectively induced the degradation of PD-L1 protein in various malignant cells in a proteasome-dependent manner. Moreover, compound 21a could significantly reduce PD-L1 protein levels of MC-38 cancer cells in vivo, by which promoted the invasion of CD8+ T cells and inhibited the growth of MC-38 in vivo. This PROTAC molecule could be used as a novel and alternative strategy for cancer immunotherapy.

In pursuit of a selective hepatocellular carcinoma therapeutic agent: Novel thalidomide derivatives with antiproliferative, antimigratory and STAT3 inhibitory properties

Advanced stage liver cancer is predominantly treated with the multi-kinase inhibitor sorafenib; however, this therapeutic agent lacks selectivity in its cytotoxic actions and is associated with poor survival outcomes. Herein we report the design and preparation of several thalidomide derivatives, including a variety of novel thioether-containing forms that are especially rare in the literature. Importantly, two of the derivatives described are potent antiproliferative agents with dose-dependent selectivity for tumorigenic liver progenitor cells (LPC) growth inhibition (up to 36% increase in doubling time at 10 μM) over non-tumorigenic cells (no effect at 10 μM). Furthermore, these putative anti-liver cancer agents were also found to be potent inhibitors of tumorigenic LPC migration. This report also describes these derivatives’ effects on several key signalling pathways in our novel liver cell lines by immunofluorescence and AlphaLISA assays. Aryl thioether derivative 7f significantly reduced STAT3 phosphorylation (23%) and its nuclear localisation (16%) at 10 μM in tumorigenic LPCs, implicating the IL-6/JAK/STAT3 axis is central in the mode of action of our derivatives.