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21172-31-6

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21172-31-6 Usage

General Description

2-(3-(Trifluoromethyl)phenyl)acetaldehyde, also known as TFPAA, is a chemical compound with the molecular formula C9H7F3O. It is a colorless liquid with a pungent, fruity odor and is commonly used as an intermediate in the production of pharmaceuticals and agrochemicals. TFPAA is also utilized as a flavor and fragrance ingredient in the food and beverage industry. It is known for its strong oxidizing properties and is considered to be mildly hazardous if ingested, inhaled, or absorbed through the skin. Due to its potential health risks, TFPAA should be handled and stored with caution in a controlled environment.

Check Digit Verification of cas no

The CAS Registry Mumber 21172-31-6 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,1,1,7 and 2 respectively; the second part has 2 digits, 3 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 21172-31:
(7*2)+(6*1)+(5*1)+(4*7)+(3*2)+(2*3)+(1*1)=66
66 % 10 = 6
So 21172-31-6 is a valid CAS Registry Number.

21172-31-6SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 14, 2017

Revision Date: Aug 14, 2017

1.Identification

1.1 GHS Product identifier

Product name 2-[3-(trifluoromethyl)phenyl]acetaldehyde

1.2 Other means of identification

Product number -
Other names -

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:21172-31-6 SDS

21172-31-6Relevant articles and documents

PIPERIDINE-2,6-DIONES AS SMALL MOLECULE DEGRADERS OF HELIOS AND METHODS OF USE

-

Paragraph 00204-00206, (2021/11/26)

Disclosed are compounds and pharmaceutically acceptable salts, hydrates, solvates, prodrugs, stereoisomers, and tautomers thereof that may cause degradation of various proteins e.g., IKZF2 (Helios). Also disclosed are pharmaceutical compositions containin

Maleimide-assisted anti-Markovnikov Wacker-type oxidation of vinylarenes using molecular oxygen as a terminal oxidant

Nakaoka, Sonoe,Murakami, Yuka,Kataoka, Yasutaka,Ura, Yasuyuki

supporting information, p. 335 - 338 (2016/01/09)

Arylacetaldehydes were successfully synthesized by the anti-Markovnikov Wacker-type oxidation of vinylarenes using 1 atm O2 as a terminal oxidant under mild conditions. Electron-deficient alkenes, such as maleic anhydride and maleimides, were effective additives and would operate as ligands to stabilize the Pd(0) species during the reaction.

N-Propynyl analogs of β-phenylethylidenehydrazines: Synthesis and evaluation of effects on glycine, GABA, and monoamine oxidase

MacKenzie, Erin M.,Fassihi, Afshin,Davood, Asghar,Chen, Qiao-Hong,Rauw, Gillian,Rauw, Gail,Knaus, Edward E.,Baker, Glen B.

experimental part, p. 8254 - 8263 (2009/04/07)

A group of β-phenylethylidenehydrazines possessing a variety of substituents (Me, OMe, Cl, F, and CF3) at the ortho-, meta-, or para-positions of the phenyl ring, in conjunction with either a N-bis-(2-propynyl) or a N-mono-(2-propynyl) moiety, were synthesized and compared to the novel neuroprotective drug β-phenylethylidenehydrazine (PEH) with regard to their ability to inhibit the enzymes GABA-transaminase (GABA-T) and monoamine oxidase (MAO)-A and -B in vitro in brain tissue. Two of the analogs synthesized (mono- and bis-N-propynylPEH) were also studied ex vivo in rats to compare their effects to those of PEH with regard to ability to inhibit GABA-T and MAO and to change brain levels of several important amino acids. Unlike PEH, none of the new drugs inhibited GABA-T in vitro at 10 or 100 μM, and all of the drugs (including PEH) were poor inhibitors (at 10 μM) of MAO-A and -B in vitro. The two analogs studied ex vivo inhibited GABA-T to a lesser extent than PEH, unlike PEH that did not elevate brain levels of GABA, and inhibited MAO-A and -B more potently than PEH. Interestingly, unlike PEH, the two analogs caused marked increases in brain levels of glycine; because of the current interest in drugs that increase glycine availability in the brain as potential antipsychotic drugs, these two analogs now warrant further investigation.

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