1085412-36-7

Basic information

• Product Name: CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester
• Synonyms: CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester;tert-butyl 2-(2-aMinoquinolin-4-yloxy)ethylcarbaMate
• CAS NO: 1085412-36-7
• Molecular Formula: C₁₆H₂₁N₃O₃
• Molecular Weight: 303.35624
• Mol File: 1085412-36-7.mol
• Article Data: 6

Chemical Properties

• Appearance: /
• Storage Temp.: 2-8°C(protect from light)
• CAS DataBase Reference: CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester(CAS DataBase Reference)
• NIST Chemistry Reference: CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester(1085412-36-7)
• EPA Substance Registry System: CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester(1085412-36-7)

Safety Data

• Hazardous Substances Data: 1085412-36-7(Hazardous Substances Data)

Usage

General Description

CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester is a chemical compound with the molecular formula C21H28N4O4. It is a carbamate derivative with potential antineoplastic activity. CarbaMic acid, N-[2-[(2-aMino-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester is believed to inhibit DNA topoisomerase II, an enzyme necessary for DNA replication and transcription, which may lead to apoptosis in cancer cells. Additionally, this compound has shown potential as a treatment for multidrug-resistant tumors. Further research is needed to fully understand the potential therapeutic applications of CarbaMic acid, N-[2-[(2-aMin-4-quinolinyl)oxy]ethyl]-, 1,1-diMethylethyl ester in the treatment of cancer and other diseases.

Upstream product

• 26690-80-2 2-(N-tert-butoxycarbonylamino)ethanol 
• 42712-64-1 2-amino-quinolin-4-ol 
• 343868-71-3 2-amino-1,4-dihydroquinolin-4-one 

Downstream Products

• 1472611-44-1 4-(2-aminoethoxy)-N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)pyridine-2,6-dicarboxamide tris(trifluoroacetate) 
• 1393488-53-3 C₄₀H₃₆N₁₀O₇ 
• 1595051-11-8 C₄₈H₅₂Cl₂N₁₂O₆ 

Relevant articles and documents

Controlled-folding of a small molecule modulates DNA G-quadruplex recognition

Differential recognition of diverse G-quadruplex structures can be achieved by controlling the folding of a small molecule. The Royal Society of Chemistry.

Reprogramming the mechanism of action of chlorambucil by coupling to a G-quadruplex ligand

The nitrogen mustard Chlorambucil (Chl) generates covalent adducts with double-helical DNA and inhibits cell proliferation. Among these adducts, interstrand cross-links (ICLs) are the most toxic, as they stall replication by generating DNA double strand breaks (DSBs). Conversely, intrastrand cross-links generated by Chl are efficiently repaired by a dedicated Nucleotide Excision Repair (NER) enzyme. We synthesized a novel cross-linking agent that combines Chl with the G-quadruplex (G4) ligand PDS (PDS-Chl). We demonstrated that PDS-Chl alkylates G4 structures at low μM concentrations, without reactivity toward double- or single-stranded DNA. Since intramolecular G4s arise from a single DNA strand, we reasoned that preferential alkylation of such structures might prevent the generation of ICLs, while favoring intrastrand cross-links. We observed that PDS-Chl selectively impairs growth in cells genetically deficient in NER, but did not show any sensitivity to the repair gene BRCA2, involved in double-stranded break repair. Our findings suggest that G4 targeting of this clinically important alkylating agent alters the overall mechanism of action. These insights may inspire new opportunities for intervention in diseases specifically characterized by genetic impairment of NER, such as skin and testicular cancers.

Pyridostatin analogues promote telomere dysfunction and long-term growth inhibition in human cancer cells

The synthesis, biophysical and biological evaluation of a series of G-quadruplex interacting small molecules based on a N,N′-bis(quinolinyl) pyridine-2,6-dicarboxamide scaffold is described. The synthetic analogues were evaluated for their ability to stabilize telomeric G-quadruplex DNA, some of which showed very high stabilization potential associated with high selectivity over double-stranded DNA. The compounds exhibited growth arrest of cancer cells with detectable selectivity over normal cells. Long-time growth arrest was accompanied by senescence, where telomeric dysfunction is a predominant mechanism together with the accumulation of restricted DNA damage sites in the genome. Our data emphasize the potential of a senescence-mediated anticancer therapy through the use of G-quadruplex targeting small molecules based on the molecular framework of pyridostatin.