Product Name:Ethyl 1-benzyl-3-oxopiperidine-4-carboxylate

IUPAC Name:ethyl 1-benzyl-3-oxopiperidine-4-carboxylate

CAS:39514-19-7
Molecular Formula:C15H19NO3
Purity:95%+
Catalog Number:CM181043
Molecular Weight:261.32

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CM181043-25g in stock ǧɅƱ
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Product Details

CAS NO:39514-19-7
Molecular Formula:C15H19NO3
Melting Point:-
Smiles Code:CCOC(=O)C1CCN(CC2=CC=CC=C2)CC1=O
Density:
Catalog Number:CM181043
Molecular Weight:261.32
Boiling Point:368.6°C at 760 mmHg
MDL No:MFCD00044512
Storage:Keep in dark place.Store at 5°C~15°C

Category Infos

Piperidines
Piperidine is an azacycloalkane that is cyclohexane in which one of the carbons is replaced by a nitrogen. Although piperidine is a common organic compound, it is an immensely important class of compounds medicinally: the piperidine ring is the most common heterocyclic subunit among FDA approved drugs.
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Benzenes
Benzene is an important organic compound with the chemical formula C6H6, and its molecule consists of a ring of 6 carbon atoms, each with 1 hydrogen atom. Benzene is a sweet, flammable, colorless and transparent liquid with carcinogenic toxicity at room temperature, and has a strong aromatic odor. It is insoluble in water, easily soluble in organic solvents, and can also be used as an organic solvent itself. The ring system of benzene is called benzene ring, and the structure after removing one hydrogen atom from the benzene ring is called phenyl. Benzene is one of the most important basic organic chemical raw materials. Many important chemical intermediates can be derived from benzene through substitution reaction, addition reaction and benzene ring cleavage reaction.

Column Infos

Adagrasib
Jan. 10, 2024, EC approves KRAZATI (adagrasib) as a targeted treatment option for patients with advanced non-small cell lung cancer (NSCLC) with a KRAS G12C mutation.
Adagrasib is an orally available, potent, irreversible, small molecule inhibitor of KRAS G12C mutant isoform for the treatment of solid tumours harbouring KRAS G12C oncogenic driver mutation. Adagrasib covalently binds to the mutant cysteine in KRAS G12C and locks the mutant KRAS protein in its inactive state, thereby preventing downstream signalling without affecting wild-type KRAS protein.

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