Pheneturide is an anticonvulsant drug that was introduced in the 1950s for the treatment of epilepsy. It is a derivative of phenobarbital and has a similar mechanism of action. Pheneturide works by enhancing the effects of GABA, an inhibitory neurotransmitter in the brain. This action helps to reduce the frequency and severity of seizures. However, pheneturide has been associated with a number of serious side effects, including liver damage, blood disorders, and psychological problems. As a result, it is no longer widely used in clinical practice. Despite its limited clinical use, pheneturide continues to be studied for its potential therapeutic applications. Some research suggests that pheneturide may have neuroprotective effects and could be beneficial in the treatment of neurodegenerative diseases, such as Alzheimer's disease. However, more research is needed to confirm these findings. Additionally, pheneturide has been shown to have anti-inflammatory properties, which could make it a potential candidate for the treatment of inflammatory disorders.'
pheneturide: product of ring hydrolysis of phenobarbital; structure; RN given refers to parent cpd without isomeric designation [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]
| ID Source | ID |
|---|---|
| PubMed CID | 72060 |
| CHEMBL ID | 2107062 |
| CHEBI ID | 31989 |
| SCHEMBL ID | 35066 |
| MeSH ID | M0047608 |
| Synonym |
|---|
| benzeneacetamide, n-(aminocarbonyl)-.alpha.-ethyl- |
| PBU , |
| s 46 |
| ethylphenylacetylurea |
| n-(aminocarbonyl)-2-phenylbutanamide |
| 1-((ethyl)phenylacetyl)urea |
| ccris 3075 |
| benuride |
| pheneturidum [inn-latin] |
| lircapyl |
| feneturida [inn-spanish] |
| urea, (2-phenylbutyryl)- |
| m 551 |
| 2-phenylbutyrylurea |
| aethylphenacemidum |
| phenuride |
| einecs 201-998-2 |
| laburide |
| phenylethylacetyluree [french] |
| n-(alpha-phenylbutyryl)urea |
| pheneturide [inn:ban] |
| urea, (2-phenylbutyryl)-, (+)- |
| d-pheneturide |
| benzeneacetamide, n-(aminocarbonyl)-alpha-ethyl-, (-)- |
| n-(aminocarbonyl)-alpha-ethylbenzeneacetamide (-)- |
| n-(aminocarbonyl)-alpha-ethylbenzeneacetamide (+)- |
| (+)-pheneturide |
| urea, (2-phenylbutyryl)-, (-)- |
| (-)-pheneturide |
| dl-pheneturide |
| benzeneacetamide, n-(aminocarbonyl)-alpha-ethyl-, (+)- |
| l-pheneturide |
| NCGC00180997-01 |
| ethylphenacemide |
| pheneturide |
| 90-49-3 |
| D01190 |
| ethylphenacemide (jan) |
| pheneturide (inn) |
| phenylethylacetylurea |
| n-carbamoyl-2-phenylbutanamide |
| 6509-32-6 |
| dtxcid40612 |
| tox21_302208 |
| dtxsid4020612 , |
| cas-90-49-3 |
| NCGC00255213-01 |
| tox21_112650 |
| CHEMBL2107062 |
| chebi:31989 , |
| m-551 |
| 6509-31-5 |
| unii-878cej4hgx |
| phenylethylacetyluree |
| pheneturidum |
| feneturida |
| 878cej4hgx , |
| 6192-36-5 |
| AKOS011976695 |
| ethylphenacemide [jan] |
| pheneturide [who-dd] |
| pheneturide [inn] |
| n-(.alpha.-phenylbutyryl)urea |
| s-46 |
| pheneturide [mart.] |
| .alpha.-phenyl-.alpha.-ethylacetylurea |
| pheneturide [mi] |
| MLS006010403 |
| smr001798871 |
| SCHEMBL35066 |
| (2-phenylbutanoyl)urea |
| n-carbamoyl-2-phenyl-butanamide |
| AJOQSQHYDOFIOX-UHFFFAOYSA-N |
| n-(2-phenylbutanoyl)urea # |
| SR-01000944857-1 |
| sr-01000944857 |
| phenylethylacetylurea (2-phenylbutyrylurea) |
| 67865-68-3 |
| n-carbamoyl-2-phenyl butanamide |
| FT-0718577 |
| DB13362 |
| Q7181340 |
| benuride; epa; ethylphenacemide; lircapyl; m 551 |
| EN300-136805 |
| AMY40721 |
| MS-23123 |
| CS-0034531 |
| HY-111177 |
| F88147 |
| Z995154698 |
| Excerpt | Reference | Relevance |
|---|---|---|
| "The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs." | ( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019) | 0.51 |
| Class | Description |
|---|---|
| amine | A compound formally derived from ammonia by replacing one, two or three hydrogen atoms by hydrocarbyl groups. |
| [compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res] | |
| Protein | Taxonomy | Measurement | Average (µ) | Min (ref.) | Avg (ref.) | Max (ref.) | Bioassay(s) |
|---|---|---|---|---|---|---|---|
| AR protein | Homo sapiens (human) | Potency | 66.8242 | 0.0002 | 21.2231 | 8,912.5098 | AID743042 |
| cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_a | Homo sapiens (human) | Potency | 76.9588 | 0.0017 | 23.8393 | 78.1014 | AID743083 |
| Cellular tumor antigen p53 | Homo sapiens (human) | Potency | 76.9588 | 0.0023 | 19.5956 | 74.0614 | AID651631 |
| [prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023] | |||||||
| Assay ID | Title | Year | Journal | Article |
|---|---|---|---|---|
| AID1346986 | P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen | 2019 | Molecular pharmacology, 11, Volume: 96, Issue:5 | A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. |
| AID1296008 | Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening | 2020 | SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1 | Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening. |
| AID1346987 | P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen | 2019 | Molecular pharmacology, 11, Volume: 96, Issue:5 | A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. |
| AID504749 | qHTS profiling for inhibitors of Plasmodium falciparum proliferation | 2011 | Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043 | Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets. |
| AID1079949 | Proposed mechanism(s) of liver damage. [column 'MEC' in source] | |||
| AID1079934 | Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source] | |||
| AID1079936 | Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source] | |||
| AID1079931 | Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source] | |||
| AID1079941 | Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source] | |||
| AID1079947 | Comments (NB not yet translated). [column 'COMMENTAIRES' in source] | |||
| AID1079943 | Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source] | |||
| AID1079935 | Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source] | |||
| AID1079945 | Animal toxicity known. [column 'TOXIC' in source] | |||
| AID1079946 | Presence of at least one case with successful reintroduction. [column 'REINT' in source] | |||
| AID1079944 | Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source] | |||
| AID1079938 | Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source] | |||
| AID1079939 | Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source] | |||
| AID1079933 | Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is | |||
| AID1079937 | Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source] | |||
| AID1079932 | Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source] | |||
| AID1079948 | Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source] | |||
| AID1079940 | Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source] | |||
| AID1079942 | Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source] | |||
| [information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||||
| Timeframe | Studies, This Drug (%) | All Drugs % |
|---|---|---|
| pre-1990 | 20 (83.33) | 18.7374 |
| 1990's | 1 (4.17) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 2 (8.33) | 24.3611 |
| 2020's | 1 (4.17) | 2.80 |
| [information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||
According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.
| This Compound (20.04) All Compounds (24.57) |
| Publication Type | This drug (%) | All Drugs (%) |
|---|---|---|
| Trials | 1 (3.70%) | 5.53% |
| Reviews | 0 (0.00%) | 6.00% |
| Case Studies | 0 (0.00%) | 4.05% |
| Observational | 0 (0.00%) | 0.25% |
| Other | 26 (96.30%) | 84.16% |
| [information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||