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Last update 08 May 2025

Promolate

Last update 08 May 2025

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Promolate (INN), Atusil

Target-

Action-

Mechanism-

Therapeutic Areas

Respiratory Diseases

Active Indication

Cough

Inactive Indication-

Originator Organization-

Active Organization-

Inactive Organization-

License Organization-

Drug Highest PhaseApproved

First Approval Date-

Regulation-

Structure/Sequence

Molecular FormulaC16H23NO4

InChIKeyGMISKEUWHIRDNK-UHFFFAOYSA-N

CAS Registry3615-74-5

100 Clinical Results associated with Promolate

100 Translational Medicine associated with Promolate

100 Patents (Medical) associated with Promolate

Literatures (Medical) associated with Promolate

Archives Internationales de Pharmacodynamie et de Therapie

Distribution and metabolic fate of morphethylbutyne in rats (2-phenoxy-isobutyric acid, 2-morpholine-ethyl ester)

Author: Marchetti, Enzo ; Bergesi, G.

The biotransformation, absorption, distribution, and excretion of morphethylbutyne (2-phenoxyisobutyric acid, 2-morpholinoethyl ester) (1000 mg/kg, oral) and of its main metabolite, 2-phenoxyisobutyric acid (PIB acid) were studied in fasted rats.Morphethylbutyne was rapidly absorbed and partially hydrolyzed by the alimentary tract so that ∼40% of the dose was detected in the stomach, small intestines, and cecum, whereas the amount of PIB acid detected in the above organs corresponded to only 5% of the administered dose.After 8 hr, no morphethylbutyne could be detected in the gastrointestinal tract and only PIB acid was found in the colon.Morphethylbutyne was rapidly hydrolyzed by tissue and serum esterases to PIB acid, which could be detected immediately in blood, liver, lungs, kidneys, and brain.The excretion of PIB acid in the urine and bile was completed within 8-24 hr and in feces within 120 hr.

Farmaco, Edizione Scientifica

Antitussive drugs

Author: Samueli, F. ; Marchetti, E. ; Mattalia, G.

I were prepared by treating α-phenoxy-, α-o-chlorophenoxy- and α-(o-methoxyphenoxy)isobutyryl chloride with the appropriate amino alcs.Thus, a solution of α-(o-chlorophenoxy)isobutyric acid in 500 ml. anhydrous C₆H₆ was added to a solution containing 133 g. N,N-dimethylaminoethoxyethanol and 202 g. of Et₃N in 500 ml. of anhydrous C₆H₆, the mixture was boiled 4 hrs. with continuous stirring; the Et₃N.HCl was filtered off; the solvent was then evaporatedI (R¹ = Cl, R² = (CH₂)₂O(CH₂)₂NMe₂ b. 130-5°.Citrate salt was prepared by addition of an alc. solution of citric acid to the product.Similarly prepared were the following I [R¹, R² (X = piperidino, Y = morpholino), b.p., and m.p. citrate salt given]: H, (CH₂)₂NMe₂, 93°, 98-9°;H, (CH₂)₂NEt₂, 105-7°, 134-5°;H, (CH₂)₂X, 122-5°, 75-8°;H, (CH₂)₂Y, 127-30°, -- (hydrochloride 143-5°); H, (CH₂)₂O(CH₂)₂NMe₂ (II), 125-8°, 84-5°; H, (CH₂)₂O(CH₂)₂NEt₂, 117-20°, 83-4°; H, (CH₂)₂O(CH₂)₂Y, 125-30°, 100-2°; Cl, (CH₂)₂NMe₂, 122-3°, 88-90°; Cl, (CH₂)₂NEt₂, 124-6°, 131-3°; Cl, (CH₂)₂X, 128-32°, 62-6°; Cl, (CH₂)₂Y, 140-2°, 85-7°; Cl, (CH₂)₂O(CH₂)₂NEt₂, 134-8°, 72-4°; Cl, (CH₂)₂O(CH₂)₂Y, 136-9°, 75-7°; MeO, (CH₂)₂NMe₂, 115-18°, 86-8°; MeO, (CH₂)₂NEt₂, 126-8°, 106-8°; MeO, (CH₂)₂X, 132-4°, 54-6°; MeO, (CH₂)₂Y, 130-5°, 100-2°; MeO, (CH₂)₂O(CH₂)₂NMe₂, 129-33°, 70-1°; MeO, (CH₂)₂O(CH₂)₂NEt₂ (III), 133-7°, 80-1°; MeO, (CH₂)₂O(CH₂)₂Y, 140-5°, 77-9°.Antitussive properties were found in II and III.

Frontiers in Molecular Biosciences

Carnitine O-octanoyltransferase (CROT) deficiency in mice leads to an increase of omega-3 fatty acids

Article

Author: Okui, Takehito ; Singh, Sasha A ; Aikawa, Elena ; Iwashita, Masaya ; Itagawa, Rei ; Kuraoka, Shiori ; Kasai, Taku ; Aikawa, Masanori

Introduction: Carnitine O-octanoyltransferase (CROT) is a well-established peroxisomal enzyme involved in liver fatty acid oxidation, but less is known about its recently discovered role in promoting vascular calcification, and whether CROT-dependent liver metabolism contributes to the latter. To date, CROT function in the context of calcification potential has been conducted in the dyslipidemic low-density lipoprotein receptor-deficient (Ldlr−/−) mice.Objectives: To differentiate peroxisome and CROT-dependent lipid biology from that of lipoprotein-mediated lipid biology, we therefore conducted a metabolomic analysis of the liver and plasma of normolipidemic CROT-deficient (Crot−/−) mice.Methods: We performed LC-MS-based metabolomics on liver and plasma derived from Crot−/− and Crot +/− mice and sibling Crot+/+ mice, using a dual-phase metabolite extraction protocol, and multiple LC-MS acquisition strategies.Results: We identified between 79 to 453 annotated metabolites from annotated metabolites from liver samples, and 117 to 424 annotated metabolites from plasma samples. Through differential abundance analysis, we determined that omega-3 fatty acids such as EPA, DPA, and DHA were higher in the liver of Crot−/− and Crot +/− mice than Crot+/+ mice. EPA were higher in plasma of Crot−/− mice than Crot+/+ mice. We also determined that the anti-inflammatory dicarboxylic acids, tetradecanedioic acid and azelaic acid, were higher in the plasma of CROT-deficient mice.Conclusion: Our study associated genetic CROT deletion with increased levels of anti-inflammatory molecules in mouse liver and plasma. These results suggest a potential mechanism for anti-calcification effects of CROT suppression and the potential use of omega-3 fatty acids as biomarkers for future CROT inhibition therapies.

100 Deals associated with Promolate

External Link

KEGG	Wiki	ATC	Drug Bank
D08433	-	R05D	-

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Cough	-	-	-

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