Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PROPIOPHENONE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1998

Antineoplastic and cytotoxic activity of beta-alkylamino-(para-substituted)propiophenone and beta-alkylamino-(6-methyl)-naphthone derivatives in murine and human tissue culture cells.

The beta-alkylamino(para-substituted)propiophenone and beta-alkylamino-(6-methyl)naphthone derivatives were evaluated for their antineoplastic effects in vitro in CF1 mice at 8 mg/kg/day intraperitoneal for 9 days. A number of these agents showed over 70% inhibition of Ehrlich ascites carcinoma growth. In in vitro cytotoxicity assays, these agents significantly inhibited the growth of a number of cancer cell lines from both human and murine origins. Some agents showed more activity than several standard anticancer drugs against certain cell lines. Three analogs, beta-(4-methyl)piperidino-(para-methyl)propiophenone (4), beta-piperidino-(para-ethoxy)propiophenone (13), and beta-hexamethyleneimino-(para-ethoxy)-propiophenone (14), were selected for mode of action studies and all showed significant inhibition of DNA and RNA syntheses at 100 microM after 60 min incubation. However, the most significant site of action was the inhibition of the activity of dihydrofolate reductase.

Animals↗
PubMed1981

The effects of cofactor and species differences on the in vitro metabolism of propiophenone and phenylacetone.

In vitro metabolism of the aromatic ketone propiophenone and its nonaromatic isomer phenylacetone was studied using fortified 12 000 X g supernatants of liver homogenates from rat and rabbit. Reduction to the corresponding alcohols was the major metabolic route observed, although aliphatic C-hydroxylation and alcohol dehydrogenation also occurred. Marked differences were observed in the amounts of carbonyl reduction of the substrates, which was dependent on the species as well as the cofactor employed. Using rat liver preparation, phenylacetone was reduced to 1-phenyl-2-propanol much more efficiently with an NADH-fortified system than when NADPH was used whereas in rabbit, extensive reduction occurred in the presence of either cofactor. Reduction of propiophenone to 1-phenyl-1-propanol by rat liver preparation was slightly greater in the presence of NADH than with NADPH; the converse was observed in rabbit. Aliphatic hydroxylation of propiophenone to 2-hydroxy-1-phenyl-1-propanone was also a significant metabolic pathway in both species, with NADPH being the more efficient cofactor, but C-1 hydroxylation of phenylacetone to 1-hydroxy-1-phenyl-2-propanone occurred only to a minor extent. Small amounts of 1-phenyl-1,2-propanedione, as well as both erythro and threo isomers of 1-phenyl-1,2-propanediol, were also identified as metabolites in both species. Similar metabolic studies were carried out on the alcohols 1-phenyl-1-propanol and 1-phenyl-2-propanol and again the nature and quantities of metabolites isolated showed both species and cofactor dependencies.

Acetone↗
PubMed1989

Degradation kinetics of (+/-)-4'-ethyl-2-methyl-3-(1-pyrrolidinyl)propiophenone hydrochloride (HY-770) and structure-stability relationship among its analogues in aqueous solution.

The kinetics and pathways for degradation of (+/-)-4'-ethyl-2-methyl-3-(1-pyrrolidinyl)propiophenone hydrochloride (HY-770; 1), a newly developed muscle-relaxing agent, and its analogues were studied in aqueous solution at 50 degrees C, ionic strength 0.5 M, and pH 8.0-12.0. Compound 1 and its four analogues followed pseudo-first-order degradation kinetics at constant pH and temperature. From the analysis of the pH degradation-rate profiles, it is evident that specific hydroxide ion-catalyzed degradations of ionized and un-ionized species occur for 1 and its structural analogue, 3'-fluoro-2-methyl-3-(1-pyrrolidinyl)propiophenone hydrochloride (HN-961; 5). The hydroxide ion-catalyzed degradation of the ionized species was found to be 100 times faster than that of the un-ionized species and to be the major process at pH less than 9.0. On the contrary, 1 was extremely stable in 0.5 M HCl at 50 degrees C, suggesting that the hydronium ion-catalyzed degradation and the spontaneous degradation of the ionized species is negligible. The Arrhenius plot for the degradation of 1 at 35-50 degrees C and pH 9.0 showed that the apparent energy of activation was 22.0 kcal/mol. The degradation rates of the five structural analogues were significantly dependent on the electron withdrawing effect of the benzene substituents of the molecule.

Boric Acids↗
PubMed1976

Metabolic interaction of secondary amines and tertiary amino propiophenones with monoamine oxidase systems.

The metabolic interaction of three secondary amines and three nitrogen-containing metabolites of safrole (tertiary amino propiophenones) with rat liver mitochondrial monoamine oxidase systems was studied in vitro employing [7-14C] benzylamine--HCl as a substrate. The two cyclic secondary amines, piperidine and pyrrolidine, showed hyperbolic competitive inhibition while pure competitive inhibition was observed in case of dimethylamine--HCl and three safrole metabolites. Inhibition characteristics for rat liver, kidney and brain mitochondrial monoamine oxidase with two cyclic secondary amines and tertiary amino with two cyclic secondary amines and tertiary amino propiophenones of safrole and elemicin were investigated manometrically using tyramine and serotonin as the substrates.

Animals↗
PubMed1997

Specific identification of Mycobacterium tuberculosis with the luciferase reporter mycobacteriophage: use of p-nitro-alpha-acetylamino-beta-hydroxy propiophenone.

We have previously described a luciferase reporter mycobacteriophage (LRP) assay that can detect Mycobacterium tuberculosis and characterize mycobacterial drug susceptibility patterns within 24 to 48 h in positive cultures. One drawback of this LRP protocol is the ability of the recombinant mycobacteriophage phAE40 to infect a variety of Mycobacterium species, thus limiting its specificity for the detection of M. tuberculosis. In this study, we have (i) explored the host range of phAE40, (ii) developed a modified LRP assay that exploits the selective inhibitory effect of the compound p-nitro-alpha-acetylamino-beta-hydroxy propiophenone (NAP) against members of the M. tuberculosis complex to differentiate between the tubercle bacillus and other mycobacterial species, and (iii) tested over 300 samples, including primary clinical isolates and drug-resistant strains of M. tuberculosis, demonstrating the ability of the NAP-modified LRP assay to identify M. tuberculosis complex organisms with high degrees of sensitivity and specificity.

Bacteriological Techniques↗
PubMed1976

Reversible adrenergic alpha-receptor blocking action of 2,4'-dimethyl-3-piperidino-propiophenone (tolperisone).

The vascular action of 2,4'-dimethyl-3-piperidino-propiophenone hydrochloride (tolperisone hydrochloride), a centrally acting muscle relaxant, was investigated in pentobarbital anesthetized dogs. Tolperisone given intravenously produced a transient hypotension, tachycardia, and hyperventilation. The drug increased the femoral arterial flow, and decreased the superior mesenteric arterial flow following an initial transient increase. When injected directly into femoral and mesenteric arteries, tolperisone caused a rapid increase in both arterial flow (vasodilatation). However, femoral vessels were about 90 times as sensitive as mesenteric vessels to tolperisone. These results indicate that tolperisone shifts the blood volume from mesenteric (visceral) vessels to femoral (skeltal) ones. The femoral vasodilatation produced by i.a. tolperisone was not depressed by the pretreatment with i.a. propranolol, atropine or chlorphenylamine. Tolperisone decreased the contractile force in an isolated and cross-circulated papillary muscle. Tolperisone produced adrenaline reversal and antagonized the pressor response to noradrenaline. Moreover, femoral vasoconstriction caused by i.a. adrenaline was converted to vasodilatation and that caused by i.a. noradrenaline was depressed during an i.a. infusion of tolperisone. These results indicate that tolperisone blocks adrenergic alpha-receptors. The blocking action was rapid in onset, short-lived, and in addition, competitive.

Adrenergic alpha-Antagonists↗
PubMed1980

[Pharmacological studies of 2-methyl-3(2-phenyl-3-methyl-tetrahydrooxazino)-propiophenone hydrochloride and 1-phenoxycarboxy-1-phenyl-2-methyl-3(2-phenyl-3-methyl-tetrahydrooxazino)-propane hydrochloride compounds].

The authors used the compounds 2-methyl-3)2-phenyl-3-methyl tetrahydroxasino)-propiophenone hydrochloriad (code PsI) and 1-phenoxycarboxy-1-phenyl-2-methyl-3 (2-phenyl-3-methyl-tetrahydroxasino-propan hydrochlorid(code P3) and carried out the following studies: influence of tripamine, corasol and strichnine seizures 1-phenoxycarboxy--1-phenyl-2-methyl--3 (2-phenyl--3-methyl-tetrahydroxasino) propar hydrochlor (Code P8) in white mice, effect on the hypertensive action of reserpine in white rats, investigations on the analeptic action in urethanized cats as well as on the analgetic effect, examined both by the test of "hot plate" and the method of Hendreshot-Forsaith. The examined compounds, administered in a dose of 1/6 of LD50, showed analgetic effect weaker than that of the preparations Morphinum hydrochloricum and Analigin, but their analeptic effect was less manifested that of of corasol. Similar to MAO-inhibitor-oproniazid although in smaller degree the compound PS1 potentiated tripamine seizures and inverted the hypotensive effect of Reserpine into hypertensive.

Analgesics↗
PubMedDate not supplied

[New, previously unavailable on the illegal drug market amphetamine derivatives with a partial propiophenone structure].

Two new clandestine synthesized derivatives of amphetamine were seized in the FRG. They show a propiophenone-structure. A well known representative of this class of compounds is 2-Diethylaminopropiohenone. The compounds are not submissed under the German law. NMR, IR- and MS-datas of these compounds and additionally synthesized derivatives are reported.

Amphetamines↗
PubMed1987

2-(N-nitroso-N-methylamino)propiophenone, a direct acting bacterial mutagen found in nitrosated Ephedra altissima tea.

A new N-nitroso compound identified in a nitrosated tea extract made from the plant Ephedra altissima and shown to be formed under in vivo conditions was identified as 2-(N-nitroso-N-methylamino)propiophenone (NMAP). N-Nitrosoephedrine (NEP), another N-nitroso compound detected in nitrosated Ephedra altissima tea and NMAP are shown to exert mutagenic activity in the Salmonella/mammalian microsome mutagenicity (Ames) test. Base-pair substitution mutation-detecting strains (TA100 and TA1535) showed both compounds to be weak direct-acting mutagens without the addition of S9-mix. The identification, synthesis and mutagenicity of NMAP are discussed.

Mutagenicity Tests↗
PubMed2004

A DFT investigation of the addition reaction of monomeric lithium enolate derived from propiophenone to propene oxide: examination of the possible transition structures.

The addition reaction of monomeric lithium enolate (Z)-1, derived from propiophenone, to propene oxide 2, was examined to clarify the exact geometry of the transition state (TS) involved in this type of reaction. The eight possible TSs and the corresponding pathways, four leading to syn gamma-hydroxy ketone (gamma-HK) 3 and four leading to anti gamma-HK 4, were compared, using the B3LYP/6-31+G(d)//B3LYP/6-31+G(d) theory level in vacuo and in the presence of the reaction solvent (toluene/hexane). In every case, the favored pathway involves a TS where the enolate C=C and the epoxide C-C are in a gauche relationship and where the Li(+) is stabilized by some C-C and C-H sigma bonds of epoxide 2.

Journal Article↗