Page last updated: 2024-12-05

hexamethylene bisacetamide

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Description

Hexamethylene bisacetamide (HMBA) is a synthetic compound with a unique structure containing two acetamide groups linked by a hexamethylene chain. It is known for its diverse biological effects, including cell cycle regulation, differentiation, and anti-cancer activity. HMBA's synthesis involves the reaction of hexamethylenediamine with acetic anhydride. Its mechanism of action is complex and involves interactions with various cellular pathways, including histone deacetylase (HDAC) inhibition. Research on HMBA has explored its potential in treating various diseases such as cancer, neurological disorders, and inflammatory diseases. Studies have demonstrated HMBA's ability to induce differentiation in cancer cells, leading to their growth arrest and apoptosis. Additionally, its anti-inflammatory effects have been observed in animal models of inflammation. Due to its intriguing biological properties and potential therapeutic applications, HMBA continues to be a subject of ongoing research.'

N,N'-diacetyl-1,6-diaminohexane: chemical name obtained from Acta Biol Hung 1990;41(1-3):199-208 [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID3616
CHEMBL ID291481
CHEBI ID125472
SCHEMBL ID61980
MeSH IDM0062259

Synonyms (77)

Synonym
MLS001074182
HMS3393E17
AKOS003422084
n,n-diacetyl-1,6-diaminohexane
hexamethylenebisacetamide
3073-59-4
NSC95580 ,
smr000059046
NCIMECH_000063
NCI60_042129
hexabid
nsc 95580
acetamide, n,n'-1,6-hexanediylbis-
diacetyldiaminohexane
brn 1775764
n,n'-1,6-hexanediylbisacetamide
ccris 7677
acetamide, n,n'-hexamethylenebis-
hexamethylenediacetamide
acetamide, n,n'-1, 6-hexanediylbis-
n,n'-hexamethylenebisacetamide
n-(6-acetamidohexyl)acetamide
n-(6-(acetylamino)hexyl)acetamide
hexamethylene bisacetamide
n, n'-diacetylhexamethylenediamine
nsc-95580
n,n'-diacetylhexamethylenediamine
acetamide,n'-1,6-hexanediylbis-
acetamide,n'-hexamethylenebis-
MLS000758275
n,n'-hexamethylene bis(acetamide), 98%
MLS000069460 ,
n,n'-diacetyl-1,6-diaminohexane
NCGC00018146-01
n,n'-hexane-1,6-diyldiacetamide
n,n'-hexamethylene-bis-acetamide
CHEBI:125472
HMS2051E17
CHEMBL291481
NCGC00018146-03
NCGC00018146-02
n-[6-(acetylamino)hexyl]acetamide
unii-la133j59vu
la133j59vu ,
4-04-00-01331 (beilstein handbook reference)
MLS001424034
HMS2231F06
CCG-35337
STL282666
FT-0629398
n-{6-[(1-hydroxyethylidene)amino]hexyl}ethanimidic acid
HMS3371N10
SCHEMBL61980
NC00059
n,n'-hexamethylene bis(acetamide)
n,n'-(hexane-1,6-diyl)diacetamide
5D4 ,
n,n'-hexamethylenebis(acetamide)
OPERA_ID_1675
mfcd00008684
DTXSID2041044
AS-62044
n,n'-1,6-hexanediylbis-acetamide
n-(6-(acetylamino)hexyl)acetamide (acd/name 4.0)
n,n'-hexamethylenebis-acetamide
hexamethylene biscetamide
J-018089
Q3732771
hexamethylene bis(acetamide)
AMY202003295
acetamide,n,n'-1,6-hexanediylbis-
D81997
A876102
n,n-hexamethylenebis(acetamide), (n,n-diacetyl-1,6-hexadiamine)
SB77455
CS-0086103
HY-124284

Research Excerpts

Overview

Hexamethylene Bisacetamide (HMBA) is a hybrid polar compound originally developed as a differentiation inducing agent. It has been discovered to have antineoplastic activity by up-regulating the expression of an endogenous antiproliferative breast cancer protein, HEXIM1.

ExcerptReferenceRelevance
"Hexamethylene Bisacetamide (HMBA) is a hybrid polar compound originally developed as a differentiation inducing agent. "( Hexamethylene bisacetamide (HMBA) simultaneously targets AKT and MAPK pathway and represses NF kappaB activity: implications for cancer therapy.
Dey, A; Kua, N; Lane, D; Teo, HL; Tergaonkar, V; Wong, E, 2008
)
3.23
"Hexamethylene bisacetamide (HMBA) is a polar compound which has recently been discovered to have antineoplastic activity by up-regulating the expression of an endogenous antiproliferative breast cancer protein, HEXIM1 (hexamethylene bisacetamide inducible protein 1) in vivo. "( Determination of hexamethylene bisacetamide, an antineoplastic compound, in mouse and human plasma by LC-MS/MS.
Ketchart, W; Montano, MM; Smith, KM; Xu, Y; Zhou, X, 2011
)
2.15
"Hexamethylene bisacetamide (HMBA) is a potent inducer of cell differentiation and HIV production in chronically infected cells. "( HMBA releases P-TEFb from HEXIM1 and 7SK snRNA via PI3K/Akt and activates HIV transcription.
Barboric, M; Contreras, X; Lenasi, T; Peterlin, BM, 2007
)
1.78
"Hexamethylene bisacetamide (HMBA) is a potent in vitro differentiating agent that has clinical potential as an anticancer drug both as a single agent and as a component of combination therapy. "( Simultaneous measurement of the cell-differentiating agent hexamethylene bisacetamide and its metabolites by gas chromatography.
Chun, HG; Kelley, JA; Roth, JS; Ward, FT, 1994
)
1.97
"Hexamethylene bisacetamide (HMBA) is a potent inducer of differentiation of a number of transformed cell lines in vitro. "( Hexamethylene bisacetamide in myelodysplastic syndrome and acute myelogenous leukemia: a phase II clinical trial with a differentiation-inducing agent.
Andreeff, M; Ervin, T; Kufe, D; Marks, PA; Michaeli, J; Rifkind, RA; Sogoloff, H; Stone, R; Tong, WP; Young, CW, 1992
)
3.17
"Hexamethylene bisacetamide (HMBA) is a potent inducer of differentiation of tumor cells. "( Enhanced replication of herpes simplex virus by hexamethylene bisacetamide.
Harada, K; Iga, H; Kondo, Y; Sato, M; Tujimoto, H; Yanagawa, T; Yoshida, H; Yura, Y, 1991
)
1.98
"Hexamethylene bisacetamide (HMBA) is a potent inducer of differentiation of murine erythroleukemia cells (MELC). "( Conversion of differentiation inducer resistance to differentiation inducer sensitivity in erythroleukemia cells.
Chen, ZX; Lebedev, YB; Marks, PA; Michaeli, J; Richon, VM; Rifkind, RA, 1990
)
1.72
"Hexamethylene bisacetamide (HMBA) is a most effective compound as an inducer of MELC differentiation. "( Induced differentiation of murine erythroleukemia cells (MELC) by polar compounds: marked increased sensitivity of vincristine resistant MELC.
Jackson, J; Marks, PA; Michaeli, J; Richon, VM; Rifkind, RA, 1989
)
1.72

Treatment

Treatment with hexamethylene bisacetamide (HMBA) increased expression of both gC protein and gC mRNA. Treatment with HMBA combined with ATRA enhances ATRA-induced differentiation in NB4-CI and arsenic-resistant NB4/As cells.

ExcerptReferenceRelevance
"Hexamethylene bisacetamide treatment promoted the cytopathic effect of R849 and increased the proportion of dead cells."( Enhancement of antitumor activity of herpes simplex virus gamma(1)34.5-deficient mutant for oral squamous cell carcinoma cells by hexamethylene bisacetamide.
Ikuta, K; Iwai, S; Naito, S; Nakazawa, M; Obayashi, S; Sumi, T; Yura, Y, 2006
)
1.26
"Treatment with hexamethylene bisacetamide (HMBA) increased expression of both gC protein and gC mRNA."( Discordant varicella-zoster virus glycoprotein C expression and localization between cultured cells and human skin vesicles.
Carpenter, JE; Grose, C; Jackson, W; Storlie, J, 2008
)
0.69
"Treatment with hexamethylene bisacetamide (HMBA) combined with ATRA enhances ATRA-induced differentiation in ATRA-insensitive NB4-CI and arsenic-resistant NB4/As cells, and is associated with stabilization of PML-RARalpha protein and increased deltaPML-RARalpha formation."( The cleavage product deltaPML-RARalpha contributes to all-trans retinoic acid-mediated differentiation in acute promyelocytic leukemia cells.
Jing, Y; Lu, M; Waxman, S; Xia, L, 2003
)
0.66
"Treatment with hexamethylene bisacetamide (HMBA), a differentiation inducing and poly (ADP-ribose)-synthesis modifying substance, influences expression of multilayered foci in a treatment schedule-dependent manner."( Modification of transformation of C3H/10T1/2 cells by a differentiation-inducing substance.
Schneider, M, 1990
)
0.62

Toxicity

ExcerptReferenceRelevance
" Daunomycin proved to be more toxic to differentiated Friend cells than to their undifferentiated counterparts."( Enhancement of daunomycin toxicity by the differentiation inducer hexamethylene bisacetamide in erythroleukemia cells.
Marcocci, L; Mavelli, I; Mondovì, B; Pedersen, JZ; Pietrangeli, P; Steinkühler, C, 1994
)
0.53

Pharmacokinetics

ExcerptReferenceRelevance
" Pharmacokinetic parameters for hexamethylene bisacetamide and plasma concentrations of the two major metabolites, N-acetyl-1,6-diaminohexane and 6-acetamidohexanoic acid, were similar for either route of administration in individual patients."( Phase I bioavailability and pharmacokinetic study of hexamethylene bisacetamide (NSC 95580) administered via nasogastric tube.
Chun, HG; Kelley, JA; Leyland-Jones, B; Lombardo, FA; Roth, JS; Ward, FT; Weiss, RB, 1991
)
0.81

Bioavailability

ExcerptReferenceRelevance
" Hexamethylene bisacetamide was rapidly absorbed from the gastrointestinal tract with a mean measured bioavailability of 99 +/- 15%."( Phase I bioavailability and pharmacokinetic study of hexamethylene bisacetamide (NSC 95580) administered via nasogastric tube.
Chun, HG; Kelley, JA; Leyland-Jones, B; Lombardo, FA; Roth, JS; Ward, FT; Weiss, RB, 1991
)
1.44
" Oral bioavailability was good (32%), with peak plasma concentrations of 2 mM achieved one hour after oral administration."( Distribution, elimination, metabolism and bioavailability of hexamethylenebisacetamide in rats.
Kelley, JA; Litterst, CL; Roth, JS, 1985
)
0.27

Dosage Studied

ExcerptRelevanceReference
" An adaptive control dosing algorithm was used to maintain HMBA steady-state concentrations (Css) within a narrow therapeutic window (1-2 mM) for five days every four weeks."( Hexamethylene bisacetamide in myelodysplastic syndrome: effect of five-day exposure to maximal therapeutic concentrations.
Auerbach, M; Conley, BA; Donehower, RC; Jones, RJ; Rowinsky, EK; Spivak, JL, 1992
)
1.73
" HMBA also induced HT29 cells to lose the capacity for anchorage-independent growth with a similar dose-response curve and time course to the loss of 29-15 epitope."( Heterogeneous responses of human colon carcinomas to hexamethylene bisacetamide.
Carnright, K; Friedman, EA; Schroy, PC; Winawer, SJ, 1988
)
0.52
"6 g/m2/day), we attempted to individualize each patient's dose based on a dosing scheme using an adaptive (feedback) control algorithm, which assumed linear clearance for HMBA."( Phase I trial using adaptive control dosing of hexamethylene bisacetamide (NSC 95580).
Conley, BA; Egorin, MJ; Forrest, A; Sinibaldi, V; Van Echo, DA; Zuhowski, EG, 1989
)
0.53
" In this dose-finding and pharmacokinetic study, five dosage levels were explored from 12 to 28 g/m2/day."( Phase I trial and clinical pharmacological evaluation of hexamethylene bisacetamide administration by ten-day continuous intravenous infusion at twenty-eight-day intervals.
Baltzer, L; Declan Walsh, T; Fanucchi, MP; Gordon, C; Marks, PA; Rifkind, RA; Stevens, YW; Tong, W; Yaldaei, S; Young, CW, 1988
)
0.52
"Salivary and plasma concentrations of hexamethylene bisacetamide (HMBA) were studied to determine (1) how the concentrations of HMBA achieved in saliva compared with those required to induce differentiation in vitro, and (2) whether saliva might substitute for plasma as a biologic fluid on which to base dosage adjustment."( Salivary concentrations of hexamethylene bisacetamide (HMBA) in patients receiving 5-day continuous infusions.
Conley, BA; Egorin, MJ; Peterson, DE; Sinibaldi, VJ; Zuhowski, EG, 1988
)
0.84
" The fraction of dose excreted in urine as AcHA was not affected by HMBA dosage and accounted for 12."( Plasma pharmacokinetics and urinary excretion of hexamethylene bisacetamide metabolites.
Callery, PS; Cohen, AS; Egorin, MJ; Geelhaar, LA; Van Echo, DA; Zuhowski, EG, 1987
)
0.53
" After oral dosing urinary excretion and plasma decay were comparable to similar data obtained after iv dosing."( Distribution, elimination, metabolism and bioavailability of hexamethylenebisacetamide in rats.
Kelley, JA; Litterst, CL; Roth, JS, 1985
)
0.27
" Despite such a down regulation of phorbol ester receptors, these cells respond to PMA with a dose-response similar to that of their parent cells, which have the normal number of phorbol ester receptors."( Continuous suppression of globin gene expression and differentiation of Friend erythroleukemia cells by phorbol 12-myristate 13-acetate (PMA) despite the loss of PMA binding sites by down regulation.
Fusco, A; Martel, N; Ostertag, W; Yamasaki, H, 1984
)
0.27
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
acetamidesCompounds with the general formula RNHC(=O)CH3.
[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]

Pathways (1)

PathwayProteinsCompounds
Initiation of transcription and translation elongation at the HIV-1 LTR01

Protein Targets (8)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Beta-lactamaseEscherichia coli K-12Potency100.00000.044717.8581100.0000AID485294
Chain A, 2-oxoglutarate OxygenaseHomo sapiens (human)Potency4.46680.177814.390939.8107AID2147
hypoxia-inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor)Homo sapiens (human)Potency12.58930.00137.762544.6684AID914; AID915
IDH1Homo sapiens (human)Potency29.09290.005210.865235.4813AID686970
chromobox protein homolog 1Homo sapiens (human)Potency100.00000.006026.168889.1251AID540317
mitogen-activated protein kinase 1Homo sapiens (human)Potency6.30960.039816.784239.8107AID1454
gemininHomo sapiens (human)Potency1.25890.004611.374133.4983AID624297
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Bile salt export pumpHomo sapiens (human)IC50 (µMol)1,000.00000.11007.190310.0000AID1449628
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (22)

Processvia Protein(s)Taxonomy
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (8)

Processvia Protein(s)Taxonomy
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (12)

Processvia Protein(s)Taxonomy
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (58)

Assay IDTitleYearJournalArticle
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
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]
AID1071775Induction of HEXIM1 protein expression in human LNCAP cells at 5 mM after 24 hrs by Western blotting analysis relative to control2014Bioorganic & medicinal chemistry letters, Mar-01, Volume: 24, Issue:5
Lead optimization of HMBA to develop potent HEXIM1 inducers.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' 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]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID82486Differentiation studies was conducted with the HL-60 human myeloid leukemia cell line and Total cells were counted with a Coulter counter, at a concentration of 3.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID82478Percent of viability for HL-60 cells was determined by dividing number of viable differentiated cells by total number of viable cells, at concentration of 3.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
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]
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID82011Percent of differentiated HL-60 cells was determined by dividing number of viable differentiated cells by total number of viable cells, at a concentration of 2.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
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]
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
AID648560Upregulation of beta-major globin gene expression in MEL cells at 5 mM after 24 to 96 hrs by RT-PCR analysis2012European journal of medicinal chemistry, Apr, Volume: 50Bis-pyrrolyl-tetrazolyl derivatives as hybrid polar compounds: A case of lipophilic functional bioisosterism with bis-acetamides.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID82487Differentiation studies was conducted with the HL-60 human myeloid leukemia cell line and Total cells were counted with a Coulter counter, at a concentration of 4.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1071768Induction of HEXIM1 protein expression in human LNCAP cells at 1 mM after 24 hrs by Western blotting analysis relative to control2014Bioorganic & medicinal chemistry letters, Mar-01, Volume: 24, Issue:5
Lead optimization of HMBA to develop potent HEXIM1 inducers.
AID1071769Induction of HEXIM1 protein expression in human LNCAP cells at 0.5 mM after 24 hrs by Western blotting analysis relative to control2014Bioorganic & medicinal chemistry letters, Mar-01, Volume: 24, Issue:5
Lead optimization of HMBA to develop potent HEXIM1 inducers.
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID82491Differentiation studies was conducted with the HL-60 human myeloid leukemia cell line and total cells were counted with a Coulter counter, at a concentration of 2.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
AID82480Percent of viability for HL-60 cells was determined by dividing number of viable differentiated cells by total number of viable cells, at concentration of 4.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
AID82142Percent of differentiated HL-60 cells was determined by dividing number of viable differentiated cells by total number of viable cells, at a concentration of 3.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID648558Induction of cell differentiation in MEL cells assessed as hemoglobin accumulation at 5 mM by after 24 to 96 hrs by spectrophotometry2012European journal of medicinal chemistry, Apr, Volume: 50Bis-pyrrolyl-tetrazolyl derivatives as hybrid polar compounds: A case of lipophilic functional bioisosterism with bis-acetamides.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID82144Percent of differentiated HL-60 cells was determined by dividing number of viable differentiated cells by total number of viable cells, at a concentration of 4.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID82350Percent of viability for HL-60 cells was determined by dividing number of viable differentiated cells by total number of viable cells, at concentration of 2.0 mM1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Chemical differentiating agents. Differentiation of HL-60 cells by hexamethylenebis[acetamide] analogues.
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]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1224864HCS microscopy assay (F508del-CFTR)2016PloS one, , Volume: 11, Issue:10
Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (552)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990199 (36.05)18.7374
1990's224 (40.58)18.2507
2000's86 (15.58)29.6817
2010's36 (6.52)24.3611
2020's7 (1.27)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 19.61

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 Index19.61 (24.57)
Research Supply Index6.35 (2.92)
Research Growth Index4.32 (4.65)
Search Engine Demand Index23.28 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (19.61)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials3 (0.53%)5.53%
Reviews31 (5.48%)6.00%
Case Studies2 (0.35%)4.05%
Observational0 (0.00%)0.25%
Other530 (93.64%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]