Page last updated: 2024-12-06

milacemide

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

milacemide: ampakine activity at AMPA Receptors; structure given in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID53569
CHEMBL ID75838
SCHEMBL ID194513
MeSH IDM0117820

Synonyms (31)

Synonym
CHEMBL75838 ,
2-pentylamino-acetamide
2-pentylamino-acetamide(milacemide)
bdbm50046768
glyzac
cp-1552-s
milacemide
glyzan
milacemide [inn]
2-(pentylamino)acetamide
milacemidum [latin]
acetamide, 2-(pentylamino)-
milacemida [spanish]
2-n-pentylaminoacetamide
AKOS000251416
76990-56-2
milacemidum
0hxt24recu ,
milacemida
unii-0hxt24recu
SCHEMBL194513
DTXSID10227786
smr004703294
MLS006011519
Z104536260
SR-01000945041-1
sr-01000945041
Q5676259
A937466
BDA99056
EN300-128867

Research Excerpts

Overview

Milacemide is a glycinamide derivative which readily enters the brain and is metabolised to glycine. It is both an inhibitor and a substrate for monoamine oxidase-type B (MAO-B) and also an inhibitor of MAO-type A (MAo-A) Milacemid has reported antiepileptic antimyoclonic properties.

ExcerptReferenceRelevance
"Milacemide is a glycinamide derivative which readily enters the brain and is metabolised to glycine. "( A microdialysis study of glycinamide, glycine and other amino acid neurotransmitters in rat frontal cortex and hippocampus after the administration of milacemide, a glycine pro-drug.
Doheny, MH; Nagaki, S; Patsalos, PN, 1996
)
1.94
"1. Milacemide is a glycine prodrug which is both an inhibitor and a substrate for monoamine oxidase-type B (MAO-B) and also an inhibitor of MAO-type A (MAO-A). "( Effect of milacemide on extracellular and tissue concentrations of dopamine and 5-hydroxytryptamine in rat frontal cortex.
Curzon, G; Doheny, M; Patsalos, PN; Sarna, G; Semba, J, 1992
)
1.31
"Milacemide is a glycine prodrug with reported antiepileptic antimyoclonic properties. "( Monoamine oxidase inhibitory properties of milacemide in rats.
Diamond, B; Fahn, S; Mena, MA; Pezzoli, G; Truong, DD, 1989
)
1.98

Effects

ExcerptReferenceRelevance
"Milacemide has a low toxicity (LD50: 2585 mg/kg in the mouse) and alters the behaviour of mouse, rat and monkey, only at high doses (greater than or equal to 1000 mg/kg)."( Anticonvulsant activity of milacemide.
Barris, D; Cordi, A; Roba, J; van Dorsser, W, 1983
)
1.28
"Milacemide has a low toxicity (LD50: 2585 mg/kg in the mouse) and alters the behaviour of mouse, rat and monkey, only at high doses (greater than or equal to 1000 mg/kg)."( Anticonvulsant activity of milacemide.
Barris, D; Cordi, A; Roba, J; van Dorsser, W, 1983
)
1.28

Treatment

ExcerptReferenceRelevance
"Milacemide-treated SDAT patients did not show significant improvement in any of the outcome measures used. "( Milacemide: a placebo-controlled study in senile dementia of the Alzheimer type.
Dysken, MW; Fakouhi, JD; Herting, RL; LeWitt, P; Mendels, J; Pomara, N; Reisberg, B; Skare, S; Wood, J, 1992
)
3.17

Pharmacokinetics

ExcerptReferenceRelevance
" Tmax and t1/2 were significantly increased and Cmax and AUC values were decreased for glycinamide compared to controls."( Antiepileptic drug pharmacokinetics and neuropharmacokinetics in individual rats by repetitive withdrawal of blood and cerebrospinal fluid: milacemide.
Curzon, G; Patsalos, PN; Semba, J, 1993
)
0.49

Dosage Studied

ExcerptRelevanceReference
" Milacemide was initiated at 800 mg/day and was gradually increased to a maximum dosage of 2,400 mg/day."( A therapeutic trial of milacemide in myoclonus and the stiff-person syndrome.
Brown, P; Day, BL; Marsden, CD; Rothwell, JC; Thompson, PD, 1991
)
1.5
" EEG-recordings, psychometric and psychophysiological tests as well as evaluation of pulse, blood pressure and side effects were carried out at the hours 0, 2, 4, 6 and 8 after the administration of one single dose of 400 mg or placebo (acute effect), after 1 week's and 2 weeks' chronic administration (chronic effect), as well as after one additional superimposed dosage of 400 mg and 1,200 mg on days 8 and 15 of chronic treatment, respectively (super-imposed effect)."( Acute and subacute CNS effects of milacemide in elderly people: double-blind, placebo-controlled quantitative EEG and psychometric investigations.
Grünberger, J; Linzmayer, L; Saletu, B, 1986
)
0.55
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (1)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Amine oxidase [flavin-containing] BBos taurus (cattle)Ki1,010.00000.05401.83906.0000AID102569; AID102572
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Molecular Functions (3)

Processvia Protein(s)Taxonomy
primary amine oxidase activityAmine oxidase [flavin-containing] BBos taurus (cattle)
aliphatic amine oxidase activityAmine oxidase [flavin-containing] BBos taurus (cattle)
monoamine oxidase activityAmine oxidase [flavin-containing] BBos taurus (cattle)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (2)

Processvia Protein(s)Taxonomy
mitochondrionAmine oxidase [flavin-containing] BBos taurus (cattle)
mitochondrial outer membraneAmine oxidase [flavin-containing] BBos taurus (cattle)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (31)

Assay IDTitleYearJournalArticle
AID17044Kinetic constant (Kcat) was calculated by inhibition of monoamino oxidase B (MAO B) at saturation1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID102572Kinetic constant was calculated by inhibition of monoamino oxidase B (MAO B)1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).
AID18282Michaelis constant (Km) was calculated by inhibition of monoamino oxidase B (MAO B)1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID102569Kinetic constant (KI) was calculated by inhibition of monoamino oxidase B (MAO B)1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).
AID1079938Chronic 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]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079931Moderate 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]
AID1079936Choleostatic 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]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID74544Tested for activation of Glutamate decarboxylase; the ratio of Vmax in the presence of activators to the Vmax in the absence of activators at a concentration of 2.5 mM.1991Journal of medicinal chemistry, Jul, Volume: 34, Issue:7
3-Alkyl-4-aminobutyric acids: the first class of anticonvulsant agents that activates L-glutamic acid decarboxylase.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID230024Ratio of Kinetic constant (Kcat) / Inactivation constant (Kinact) of the MAO B1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID74542Tested for activation of Glutamate decarboxylase; the ratio of Vmax in the presence of activators to the Vmax in the absence of activators at a concentration of 1.0 mM.1991Journal of medicinal chemistry, Jul, Volume: 34, Issue:7
3-Alkyl-4-aminobutyric acids: the first class of anticonvulsant agents that activates L-glutamic acid decarboxylase.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1079933Acute 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
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID74545Tested for activation of Glutamate decarboxylase; the ratio of Vmax in the presence of activators to the Vmax in the absence of activators at a concentration of 250 uM.1991Journal of medicinal chemistry, Jul, Volume: 34, Issue:7
3-Alkyl-4-aminobutyric acids: the first class of anticonvulsant agents that activates L-glutamic acid decarboxylase.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1079935Cytolytic 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]
AID112461Anticonvulsant potency using the intravenous-BIC (bicuculline) test in mice1998Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4
Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID118595Compound was tested for anticonvulsant activity in maximal electroshock seizure(MES) test after 30 min upon intraperitoneal administration to mice at a dose of 58 mg/kg; Animals protected / Animals tested = 2/101998Journal of medicinal chemistry, Jan-01, Volume: 41, Issue:1
N-(benzyloxycarbonyl)glycine esters and amides as new anticonvulsants.
AID17046Inactivation constant (Kinact) was calculated by inhibition of monoamino oxidase B (MAO B) at saturation1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).
AID112305Compound was tested for anticonvulsant activity in maximal electroshock seizure(MES) test after 3 hours upon intraperitoneal administration to mice1998Journal of medicinal chemistry, Jan-01, Volume: 41, Issue:1
N-(benzyloxycarbonyl)glycine esters and amides as new anticonvulsants.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (62)

TimeframeStudies, This Drug (%)All Drugs %
pre-199015 (24.19)18.7374
1990's46 (74.19)18.2507
2000's1 (1.61)29.6817
2010's0 (0.00)24.3611
2020's0 (0.00)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 19.44

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.

MetricThis Compound (vs All)
Research Demand Index19.44 (24.57)
Research Supply Index4.41 (2.92)
Research Growth Index4.55 (4.65)
Search Engine Demand Index18.60 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (19.44)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials12 (17.39%)5.53%
Reviews5 (7.25%)6.00%
Case Studies1 (1.45%)4.05%
Observational0 (0.00%)0.25%
Other51 (73.91%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]