Page last updated: 2024-12-05

piperazine

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

Piperazine is a heterocyclic organic compound with the formula (CH2)4(NH)2. It is a colorless solid that is soluble in water and has a faint ammoniacal odor. Piperazine is a weak base and forms salts with acids. It is a versatile building block in organic synthesis and is used in the manufacture of pharmaceuticals, pesticides, and other industrial chemicals. The most common use of piperazine is in the treatment of parasitic infections, especially pinworms and roundworms. It acts by paralyzing the muscles of the parasites, preventing them from attaching to the intestinal wall and causing them to be expelled. Piperazine is also used as an antihistamine and as a precursor in the synthesis of other pharmaceuticals. The synthesis of piperazine involves the reaction of ethylenediamine with 1,2-dibromoethane. Piperazine is a subject of study due to its diverse pharmacological properties and its potential for use in the development of new drugs. Research in this area focuses on the synthesis of new piperazine derivatives with improved therapeutic properties, as well as on understanding the mechanism of action of piperazine and its derivatives. In addition to its medicinal applications, piperazine also finds use in various industrial applications, including the production of polymers, surfactants, and textile auxiliaries.'

Cross-References

ID SourceID
PubMed CID4837
CHEMBL ID1412
CHEBI ID28568
MeSH IDM0107342

Synonyms (197)

Synonym
BIDD:GT0273
vermex
vermizine (tn)
CHEBI:28568 ,
KBIO1_000038
DIVK1C_000038
NCIOPEN2_000984
NCIOPEN2_001111
NCIOPEN2_001269
NCIOPEN2_001151
NCIOPEN2_001031
NCIOPEN2_001033
NCIOPEN2_001024
NCIOPEN2_001071
NCIOPEN2_001073
NCIOPEN2_000988
NCIOPEN2_001231
NCIOPEN2_001262
SPECTRUM_001113
SPECTRUM5_001817
inchi=1/c4h10n2/c1-2-6-4-3-5-1/h5-6h,1-4h
ccris 5950
nsc 474
un2579
einecs 203-808-3
piperazin [german]
hsdb 1093
eraverm (van)
brn 0102555
1,4-diethylenediamine
piperazin
eraverm
piperazine ,
pyrazine, hexahydro-
uvilon
dispermine
C07973
110-85-0
worm-a-ton
piperazidine
piperazine, anhydrous
1,4-diazacyclohexane
diethyleneimine
lumbrical
nsc474
hexahydro-1,4-diazine
pipersol
wurmirazin
nsc-474
asca-trol no. 3
1,4-piperazine
wln: t6m dmtj
antiren
diethylenediamine
hexahydropyrazine
pyrazine hexahydride
piperazine, reagentplus(r), 99%
DB00592
D00807
piperazine (usp)
NCGC00094762-01
NCGC00094762-02
KBIOSS_001593
KBIO2_001593
KBIO2_006729
KBIO2_004161
NCIOPEN2_005022
NCIOPEN2_005102
NCIOPEN2_005200
NCIOPEN2_005185
NCIOPEN2_009422
NCIOPEN2_004952
NCIOPEN2_004994
NCIOPEN2_005108
NCIOPEN2_005072
NCIOPEN2_005187
NCIOPEN2_004954
NCIOPEN2_005575
NCIOPEN2_005182
NCIOPEN2_005062
NINDS_000038
NCIOPEN2_005145
NCIOPEN2_004942
NCIOPEN2_005032
NCIOPEN2_004910
NCIOPEN2_004914
NCIOPEN2_005980
NCIOPEN2_004830
NCIOPEN2_004982
NCIOPEN2_004862
NCIOPEN2_004834
NCIOPEN2_004992
NCIOPEN2_004874
NCIOPEN2_005034
NCIOPEN2_004904
SPECTRUM1500490
IDI1_000038
HMS2092A03
CHEMBL1412
AKOS000269028
piperazine anhydrous
HMS500B20
1323940-30-2
P0447
P0446
HMS1920H20
NCGC00094762-03
NCGC00094762-05
NCGC00094762-04
pze ,
tox21_202242
NCGC00259791-01
cas-110-85-0
dtxcid701164
NCGC00254077-01
tox21_113564
tox21_300104
dtxsid1021164 ,
pharmakon1600-01500490
nsc757283
nsc-757283
STL169348
S4574
anhydrous piperazine
vermizine
upixon
piperazin [germany]
FT-0673919
unii-1rtm4pal0v
5-23-01-00030 (beilstein handbook reference)
piperazine [usp]
1rtm4pal0v ,
ec 203-808-3
piperazine [un2579] [corrosive]
LF-0561
piperazine [usp-rs]
piperazine [who-dd]
trimetazidine dihydrochloride impurity g [ep impurity]
fema no. 4250
piperazine [green book]
piperazine [fhfi]
piperazine [vandf]
piperazine [mi]
piperazinum [hpus]
p02cb01
piperazine [ii]
piperazinum
piperazine [mart.]
piperazine [hsdb]
piperazine [usp monograph]
CCG-212753
CS-4381
piperzine
piprazine
piperizine
Q-201586
STR00051
exelmin (salt/mix)
vermidol (salt/mix)
tasnon (salt/mix)
un 2579
vermizine (salt/mix)
HY-B0912
AB00052073_03
mfcd00005953
piperazine, bioultra, anhydrous, >=99.0% (t)
piperazine, analytical standard
piperazine, anhydrous, >=99.0% (t)
F0001-0226
sr-05000001700
SR-05000001700-1
piperazine, united states pharmacopeia (usp) reference standard
piperazine, p.a., 98%
piperazine, 99%
piperazina
SBI-0051485.P003
Z1245537944
BCP24060
Q409292
4-diazacyclohexane
exahydropyrazine
EN300-33920
HMS3885L08
NCGC00094762-08
1,4 piperazine
1,4 diazacyclohexane
7-piperazine
piperazine-
31977-51-2
BP-31252
piperazine (mart.)
piperazine (usp monograph)
piperazine (usp-rs)
roundworm de-wormer for cats and kittens
piperazine (anhydrous)
hexahydropirazine
piperazine (ii)

Research Excerpts

Overview

Piperazine is a structural element present in drugs belonging to various chemical classes and used for numerous different therapeutic applications. Piperazine scaffold is an important fragment that is used in many currently used FDA approved drugs in different diseases including PARP1 inhibitor Olaparib.

ExcerptReferenceRelevance
"Piperazine (PIP) is a pharmaceutically acceptable molecule and a good co-conformer in crystallographic engineering. "( An Evolving Role of Aqueous Piperazine to Improve the Solubility of Non-Steroidal Anti-Inflammatory Drugs.
Du, G; Fang, Z; Gong, N; Lu, Y; Xing, C; Xing, W; Yu, H; Zhang, B, 2022
)
2.46
"Piperazine is a structural element present in drugs belonging to various chemical classes and used for numerous different therapeutic applications; it has been considered a privileged scaffold for drug design."( The piperazine scaffold for novel drug discovery efforts: the evidence to date.
Braconi, L; Dei, S; Gabellini, A; Manetti, D; Romanelli, MN; Teodori, E, 2022
)
2.72
"Piperazine scaffold is an important fragment that is used in many currently used FDA approved drugs in different diseases including PARP1 inhibitor Olaparib."( Identifying new piperazine-based PARP1 inhibitors using text mining and integrated molecular modeling approaches.
Durdagi, S; Sahin, K, 2021
)
1.69
"Piperazine scaffolds are a group of heterocyclic atoms having pharmacological values and showing significant results in pharmaceutical chemistry. "( An Overview of Piperazine Scaffold as Promising Nucleus for Different Therapeutic Targets.
Fayaz, F; Kaur, A; Khasimbi, S; Pottoo, FH; Sharma, A; Wakode, S, 2020
)
2.35
"Piperazine derivatives are an attractive class of chemical compounds for the treatment of various mental illness. "( Neuropharmacological assessment in mice and molecular docking of piperazine derivative LQFM212.
Costa, EA; da Rocha, FF; de Brito, AF; de Carvalho, FS; Fontana, C; Lião, LM; Menegatti, R; Moreira, LK; Sanz, G; Vaz, BG; Verli, H, 2020
)
2.24
"The piperazine scaffold is a privileged structure frequently found in biologically active compounds. "( Recent advances in the synthesis of piperazine based ligands and metal complexes and their applications.
Kant, R; Maji, S, 2021
)
1.45
"Piperazine (PZ) is an efficient amine for carbon capture systems, but it can form N-nitrosopiperazine (MNPZ), a carcinogen, from nitrogen oxides (NO(x)) in flue gas from coal or natural gas combustion. "( Kinetics of N-nitrosopiperazine formation from nitrite and piperazine in CO2 capture.
Fine, NA; Goldman, MJ; Rochelle, GT, 2013
)
2.15
"Piperazine derivatives are a class of psychoactive substances applied in prescription medicines like antidepressants as well as in drugs of abuse. "( Structure-dependent inhibition of the human α1β2γ2 GABAA receptor by piperazine derivatives: A novel mode of action.
Hermans, EJ; Hondebrink, L; Meulenbelt, J; Schmeink, S; van Kleef, RG; Westerink, RH, 2015
)
2.09
"Piperazine is an ideal desulfurizing agent but the heat-stable salts formed in desulfurization have caused secondary pollution and waste of resources. "( Comparative study on the regeneration of flue-gas desulfurizing agents by using conventional electrodialysis (ED) and bipolar membrane electrodialysis (BMED).
Huang, C; Xu, T, 2006
)
1.78

Effects

Piperazine has been used since the end of the nineteenth century as a urine alkalizing agent in gout and more widely in the past thirty years for its antihelmintic properties. Piperazine has a flexible core structure for the design and synthesis of new bioactive compounds.

ExcerptReferenceRelevance
"Piperazine has a flexible core structure for the design and synthesis of new bioactive compounds."( An Overview of Piperazine Scaffold as Promising Nucleus for Different Therapeutic Targets.
Fayaz, F; Kaur, A; Khasimbi, S; Pottoo, FH; Sharma, A; Wakode, S, 2020
)
1.63
"Piperazine ferulate (PF) has been reported to protect cardiac from ischemia/reperfusion injury to achieve myocardial protection. "( Piperazine ferulate protects against cardiac ischemia/reperfusion injury in rat via the suppression of NLRP3 inflammasome activation and pyroptosis.
Lei, Z; Li, B; Liu, R; Liu, Y; Luan, F; Peng, L; Peng, X; Zeng, N; Zhang, X, 2022
)
3.61
"Piperazine derivatives have been of great interest to medicinal chemists in the development of antidepressant drugs due to their distinct molecular and structural features along with their pharmacological profile. "( Design, synthesis and biological evaluation of oxadiazole clubbed piperazine derivatives as potential antidepressant agents.
Bhatia, R; Choudhary, D; Kaur, D; Kumar, B; Rawat, R; Sahu, B; Sharma, S, 2023
)
2.59
"Piperazine has a flexible core structure for the design and synthesis of new bioactive compounds."( An Overview of Piperazine Scaffold as Promising Nucleus for Different Therapeutic Targets.
Fayaz, F; Kaur, A; Khasimbi, S; Pottoo, FH; Sharma, A; Wakode, S, 2020
)
1.63
"Piperazine ferulate (PF) has been reported to exert protective effects against the progression of DN."( Piperazine ferulate attenuates high glucose‑induced mesangial cell injury via the regulation of p66
Chen, Z; Deng, RR; Xiang, DX; Yang, XD; Yang, YY; Yao, LY, 2021
)
2.79
"Piperazine has been used since the end of the nineteenth century as a urine alkalizing agent in gout and more widely in the past thirty years for its antihelmintic properties. "( [Neurologic adverse effects of piperazine].
Boissonnot, L; Gil, R; Lefevre, JP; Neau, JP; Rogez, R; Simmat, G,
)
1.86
"Piperazine has been shown to nitrosate in vivo to N-mononitrosopiperazine (MNPZ) by oral intake. "( Excretion of N-mononitrosopiperazine in urine in workers manufacturing piperazine.
Bellander, T; Hagmar, L; Osterdahl, BG; Skerfving, S, 1988
)
2.02

Toxicity

ExcerptReferenceRelevance
" To evaluate the potential toxicity of prophylactic anti- parasitic treatments on strains of mice that are commonly used as experimental models and in genetic engineering in our facility, we surveyed a number of strains and ages of mice for toxic reactions during treatment regimens that combine anthelminthic and anti-acaricidal agents."( Toxicity evaluation of prophylactic treatments for mites and pinworms in mice.
Frazier, S; Oberbeck, C; Rehg, JE; Straign, CM; Toth, LA, 2000
)
0.31
"The metabolic activation of small-molecule drugs into electrophilic reactive metabolites is widely recognized as an indicator of idiosyncratic adverse drug reactions (IADRs)."( Piperazine ring toxicity in three novel anti-breast cancer drugs: an in silico and in vitro metabolic bioactivation approach using olaparib as a case study.
Abuelizz, HA; Alsubi, TA; Attwa, MW; Darwish, HW; Kadi, AA, 2023
)
2.35

Pharmacokinetics

ExcerptReferenceRelevance
"05) and the Cmax by 57% (P<0."( Interactions of buspirone with itraconazole and rifampicin: effects on the pharmacokinetics of the active 1-(2-pyrimidinyl)-piperazine metabolite of buspirone.
Kivistö, KT; Lamberg, TS; Neuvonen, PJ, 1999
)
0.51
" Biological evaluation of these compounds focused on maintaining activity while improving pharmacokinetic (PK) properties."( Design and synthesis of piperazine-indole p38 alpha MAP kinase inhibitors with improved pharmacokinetic profiles.
Almirez, R; Chakravarty, S; Dugar, S; Hu, J; Jung, J; Laney, M; Levy, DE; Liclican, A; Lu, Q; Luedtke, GR; Mavunkel, BJ; Nashashibi, I; Perumattam, JJ; Tabora, J; Tan, X; Tester, RW; Tran, V, 2010
)
0.67
" Physiologically based pharmacokinetic (PBPK) modeling offers a means to dynamically integrate the complex interplay of the processes determining oral absorption."( Incorporation of physiologically based pharmacokinetic modeling in the evaluation of solubility requirements for the salt selection process: a case study using phenytoin.
Chiang, PC; Wong, H, 2013
)
0.39
" Pharmacokinetic studies on rats showed that the glutarate salt exhibits doubled plasma AUC values in a single dose within an hour compared to the citrate salt."( Salt and cocrystals of sildenafil with dicarboxylic acids: solubility and pharmacokinetic advantage of the glutarate salt.
Desiraju, GR; Ganguly, S; Sanphui, P; Tothadi, S, 2013
)
0.39
"The objective of the present work was to investigate the potential for pharmacokinetic drug-drug interactions between glimepiride (GMP) and piperazine dithioctate (PDT) in rats to support the development of an orally combined product of the two drugs."( Effect of Piperazine Dithioctate on the Oral Pharmacokinetics of Glimepiride in Rats.
Choi, K; Kim, EY; Lee, K; Oh, SJ; Yu, HE; Yu, K, 2015
)
1.02
" Five pharmaceutically acceptable salts, including the maleate (2), fumarate (3), citrate (4, 5), and l-malate (6) of compound 1, were prepared via the salt formation reaction and evaluated for their physicochemical and pharmacokinetic properties."( Solubility-driven optimization of benzothiopyranone salts leading to a preclinical candidate with improved pharmacokinetic properties and activity against Mycobacterium tuberculosis.
Fu, L; Gong, N; Guo, K; Huang, H; Li, G; Li, P; Lu, Y; Ma, C; Wang, B; Zhang, B, 2023
)
0.91

Compound-Compound Interactions

Piperazine ferulate (PF) combined with irbesartan could result in an improved efficacy in the treatment of DN.

ExcerptReferenceRelevance
"Seven critical tests in equids were conducted with single doses of fenbendazole (5 mg kg-1) alone (Panacur--American Hoechst, Somerville, NJ); (2 tests with paste and 1 with suspension formulation) or in combination with piperazine (American Hoechst); (40 mg base kg-1); (4 tests with paste formulation)."( Critical tests in equids with fenbendazole alone or combined with piperazine: particular reference to activity on benzimidazole-resistant small strongyles.
Drudge, JH; Lyons, ET; Tolliver, SC, 1983
)
0.69
" It is believed that piperazine ferulate (PF) combined with irbesartan could result in an improved efficacy in the treatment of DN."( Therapeutic Efficacy of Piperazine Ferulate Combined With Irbesartan in Diabetic Nephropathy: A Systematic Review and Meta-analysis.
Li, B; Li, D; Liu, R; Peng, LX; Zeng, N, 2020
)
1.18
"PF combined with irbesartan could improve the efficiency in the treatment of DN."( Therapeutic Efficacy of Piperazine Ferulate Combined With Irbesartan in Diabetic Nephropathy: A Systematic Review and Meta-analysis.
Li, B; Li, D; Liu, R; Peng, LX; Zeng, N, 2020
)
0.87

Bioavailability

Combining of xanthone with piperazine moiety resulted in compounds with increased bioavailability after oral administration.

ExcerptReferenceRelevance
"Three kinds of blended absorbents were investigated on bench-scale experimental bench according to absorption rate and regeneration grade to select a reasonable additive concentration."( [Study of new blended chemical absorbents to absorb CO2].
Cen, KF; Fang, MX; Luo, ZY; Wang, JL; Yan, SP, 2007
)
0.34
" This article describes the discovery of 2-phenyl-4-piperazinylbenzimidazoles as small molecule GnRH antagonists with nanomolar potency in in vitro binding and functional assays, excellent bioavailability (rat %F>70) and demonstrated oral activity in a rat model having shown significant serum leuteinizing hormone (LH) suppression."( 2-phenyl-4-piperazinylbenzimidazoles: orally active inhibitors of the gonadotropin releasing hormone (GnRH) receptor.
Chengalvala, M; Cottom, J; Feingold, I; Garrick, L; Green, D; Hauze, D; Huselton, C; Jetter, J; Kao, W; Kopf, GS; Lundquist, JT; Mann, C; Mehlmann, J; Pelletier, JC; Rogers, J; Shanno, L; Wrobel, J, 2008
)
0.35
" The second-order rate constant for the CO0 reaction with PZ was determined from the absorption rate measurements in the activated DEEA solutions, and its value at 303 K was found to be 24,450 m(3)/(kmol s)."( Kinetics of removal of carbon dioxide by aqueous solutions of N,N-diethylethanolamine and piperazine.
Kenig, EY; Konduru, PB; Vaidya, PD, 2010
)
0.58
" Enhanced bioavailability and preferential brain distribution make compound 6c a good candidate for pharmacological and clinical evaluation."( Synthesis and evaluation of amides surrogates of dopamine D3 receptor ligands.
Berrebi-Bertrand, I; Calmels, T; Capet, M; Danvy, D; Jean, M; Lecomte, JM; Levoin, N; Renault, J; Robert, P; Schwartz, JC; Uriac, P, 2010
)
0.36
" The lead compounds 5a, 6c, and 6e exhibited potent PAI-1 inhibitory activity and favorable oral bioavailability in the rodents."( Discovery of inhibitors of plasminogen activator inhibitor-1: structure-activity study of 5-nitro-2-phenoxybenzoic acid derivatives.
Chakrabarti, G; Chaugule, B; Jain, M; Joshi, J; Joshi, N; Pandya, V; Parmar, B; Patel, H; Patel, J; Patel, P; Rath, A; Raviya, M; Sairam, KV; Shaikh, M; Soni, H, 2011
)
0.37
"An unusually large data set of 397 piperazinyl-glutamate-pyridines/pyrimidines as potent orally bioavailable P2Y(12) antagonists for inhibition of platelet aggregation was studied for the first time based on the combination of three-dimensional quantitative structure-activity relationship (3D-QSAR), molecular docking, and molecular dynamics (MD) methods."( Combined 3D-QSAR, molecular docking, and molecular dynamics study on piperazinyl-glutamate-pyridines/pyrimidines as potent P2Y12 antagonists for inhibition of platelet aggregation.
Hao, M; Li, G; Li, Y; Wang, Y; Yan, Y; Yang, L; Zhang, S, 2011
)
0.37
"5% oral bioavailability in monkey."( Design and optimization of novel (2S,4S,5S)-5-amino-6-(2,2-dimethyl-5-oxo-4-phenylpiperazin-1-yl)-4-hydroxy-2-isopropylhexanamides as renin inhibitors.
Kato, M; Meguro, M; Miyazaki, S; Nagai, Y; Nagayama, T; Nakamura, Y; Nishi, T; Suemune, H; Sugita, C; Takahashi, M; Tamaki, K, 2012
)
0.38
" Combining of xanthone with piperazine moiety resulted in obtaining of compounds with increased bioavailability after oral administration."( Synthesis and evaluation of pharmacological properties of some new xanthone derivatives with piperazine moiety.
Bojarski, AJ; Gunia, A; Marona, H; Pytka, K; Satała, G; Siwek, A; Szkaradek, N; Szneler, E; Waszkielewicz, AM, 2013
)
0.9
"In the pharmaceutical industry, salt is commonly used to improve the oral bioavailability of poorly soluble compounds."( Incorporation of physiologically based pharmacokinetic modeling in the evaluation of solubility requirements for the salt selection process: a case study using phenytoin.
Chiang, PC; Wong, H, 2013
)
0.39
" Thus, to improve solubility and bioavailability characteristics, cocrystals and salts of the drug have been prepared by treating aliphatic dicarboxylic acids with sildenafil; the N-methylated piperazine of the drug molecule interacts with the carboxyl group of the acid to form a heterosynthon."( Salt and cocrystals of sildenafil with dicarboxylic acids: solubility and pharmacokinetic advantage of the glutarate salt.
Desiraju, GR; Ganguly, S; Sanphui, P; Tothadi, S, 2013
)
0.58
" Herein, we disclose the identification of 7-(3-(piperazin-1-yl)phenyl)pyrrolo[2,1-f][1,2,4]triazin-4-amine derivatives as highly potent, selective and orally bioavailable PI3Kδ inhibitors."( Discovery of 7-(3-(piperazin-1-yl)phenyl)pyrrolo[2,1-f][1,2,4]triazin-4-amine derivatives as highly potent and selective PI3Kδ inhibitors.
Bhide, RS; Bosnius, R; Cherney, RJ; Cornelius, LAM; Davies, P; Dhar, TGM; Goldstein, C; Gu, X; Neels, J; Poss, MA; Qin, LY; Ruan, Z; Ruepp, S; Sack, JS; Salter-Cid, L; Skala, S; Srivastava, AS; Stefanski, K; Susulic, V; Tino, JA; Weigelt, CA; Xie, J; Yang, X; Yarde-Chinn, M, 2017
)
0.46
" The SAR obtained led to the discovery of 65 (Ki = 4 nM, >1,000-fold selective for hCB1 over hCB2), an orally bioavailable aryl urea with reduced brain penetration, and provides direction for discovering peripherally restricted compounds with good in vitro and in vivo properties."( Synthesis and pharmacological characterization of functionalized 6-piperazin-1-yl-purines as cannabinoid receptor 1 (CB1) inverse agonists.
Amato, GS; Maitra, R; Manke, A; Runyon, SP; Snyder, RW; Vasukuttan, V; Wiethe, RW, 2018
)
0.48
"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
" Compared with 1, all the target salts exhibited greatly increased aqueous solubility and improved oral bioavailability in mice."( Solubility-driven optimization of benzothiopyranone salts leading to a preclinical candidate with improved pharmacokinetic properties and activity against Mycobacterium tuberculosis.
Fu, L; Gong, N; Guo, K; Huang, H; Li, G; Li, P; Lu, Y; Ma, C; Wang, B; Zhang, B, 2023
)
0.91

Dosage Studied

Four groups of two naturally infected pigs were dosed with albendazole, pyrantel pamoate, ivermectin or piperazine dihydrochloride, respectively. pigs in groups 1 and 3 were orally doses with 200 mg per kg bodyweight, the recommended dose, while pigs in group 4 were given 100 mg kg-1.

ExcerptRelevanceReference
" From the pattern of infection observed in this study it is suggested that further gains could be made by giving the second treatment at six (instead of ten) weeks of age, and by increasing the dosage of anthelmintic used."( Metaphylactic deworming program for buffalo calves (Bubalis bubalis) in North-East Thailand.
Hörchner, F; Leidl, K; Löhr, KF; Srikitjakarn, L, 1987
)
0.27
", pigs in groups 1 and 3 were orally dosed with 200 mg piperazine dihydrochloride (Ascarex D, 53%) per kg bodyweight, the recommended dose, while pigs in group 4 were given 100 mg kg-1."( The influence of high- and low-fibre diets on the activity of piperazine against Oesophagostomum spp. in pigs.
Bjørn, H; Hennessy, DR; Nansen, P; Praslicka, J, 1997
)
0.78
" Four groups of two naturally infected pigs were dosed with albendazole, pyrantel pamoate, ivermectin or piperazine dihydrochloride, respectively."( Embryonation and infectivity of Ascaris suum eggs isolated from worms expelled by pigs treated with albendazole , pyrantel pamoate, ivermectin or piperazine dihydrochloride.
Boes, J; Eriksen, L; Nansen, P, 1998
)
0.71
" cruzi infection after once daily oral dosing at 20, 50 and 100 mg/kg for 5 days."( Design, structure-activity relationship and in vivo efficacy of piperazine analogues of fenarimol as inhibitors of Trypanosoma cruzi.
Alexander, PW; Best, WM; Charman, SA; Chatelain, E; Diao, H; Gregg, AD; Keenan, M; Kerfoot, M; Khong, A; Ryan, E; Scandale, I; Shackleford, DM; Thompson, RC; von Geldern, TW; White, KL, 2013
)
0.63
" In murine infection model, TZY-5-84 at lower dosage (12."( In vitro and in vivo antimicrobial activities of a novel piperazine-containing benzothiazinones candidate TZY-5-84 against Mycobacterium tuberculosis.
Chen, X; Fu, L; Guo, S; Liu, M; Lu, Y; Wang, B; Zhao, J, 2020
)
0.8
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
anthelminthic drugSubstance intended to kill parasitic worms (helminths).
[role 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]

Drug Classes (3)

ClassDescription
piperazines
saturated organic heteromonocyclic parent
azacycloalkane
[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 Targets (16)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
GLI family zinc finger 3Homo sapiens (human)Potency3.40900.000714.592883.7951AID1259369
Microtubule-associated protein tauHomo sapiens (human)Potency28.18380.180013.557439.8107AID1468
AR proteinHomo sapiens (human)Potency63.47450.000221.22318,912.5098AID743063
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency57.58700.001022.650876.6163AID1224838; AID1224893
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency31.54360.003041.611522,387.1992AID1159552; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency22.11840.000817.505159.3239AID1159527; AID1159531
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency37.31220.001530.607315,848.9004AID1224841; AID1224849; AID1259401; AID1259403
pregnane X nuclear receptorHomo sapiens (human)Potency43.22550.005428.02631,258.9301AID1346982
estrogen nuclear receptor alphaHomo sapiens (human)Potency40.51460.000229.305416,493.5996AID1259244; AID1259248; AID743069; AID743079
67.9K proteinVaccinia virusPotency0.70790.00018.4406100.0000AID720580
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency62.93780.001723.839378.1014AID743083
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency7.92340.000323.4451159.6830AID743066
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency46.92300.000627.21521,122.0200AID743202; AID743219
Voltage-dependent calcium channel gamma-2 subunitMus musculus (house mouse)Potency70.61740.001557.789015,848.9004AID1259244
Cellular tumor antigen p53Homo sapiens (human)Potency79.23400.002319.595674.0614AID651631
Glutamate receptor 2Rattus norvegicus (Norway rat)Potency70.61740.001551.739315,848.9004AID1259244
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (124)

Processvia Protein(s)Taxonomy
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (34)

Processvia Protein(s)Taxonomy
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (20)

Processvia Protein(s)Taxonomy
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
plasma membraneGlutamate receptor 2Rattus norvegicus (Norway rat)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (34)

Assay IDTitleYearJournalArticle
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1079945Animal toxicity known. [column 'TOXIC' 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]
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
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
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]
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
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]
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]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID701844Dissociation constant, pKa of the compound2012Journal of medicinal chemistry, Jul-12, Volume: 55, Issue:13
Mitigating heterocycle metabolism in drug discovery.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID267573Antiproliferative activity against human HL60 cell line2006Journal of medicinal chemistry, Jul-13, Volume: 49, Issue:14
Antitumor activity of JS-K [O2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate] and related O2-aryl diazeniumdiolates in vitro and in vivo.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,079)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990318 (29.47)18.7374
1990's38 (3.52)18.2507
2000's163 (15.11)29.6817
2010's382 (35.40)24.3611
2020's178 (16.50)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 73.00

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 very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index73.00 (24.57)
Research Supply Index7.05 (2.92)
Research Growth Index5.10 (4.65)
Search Engine Demand Index128.99 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (73.00)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials8 (0.70%)5.53%
Reviews32 (2.81%)6.00%
Case Studies24 (2.11%)4.05%
Observational1 (0.09%)0.25%
Other1,074 (94.29%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (26)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Efficacy and Safety of a Single-dose Regimen and a Multi-dose Regimen of Mebendazole Against Hookworm Infections in School Children: a Randomized Controlled Trial [NCT03245398]Phase 4186 participants (Actual)Interventional2017-07-25Completed
Clinical Study Evaluating Mebendazole as Adjuvant Therapy in Patients With Colorectal Cancer [NCT03925662]Phase 340 participants (Anticipated)Interventional2019-04-01Recruiting
The Efficacy of a Single-dose Mebendazole Against Soil-transmitted Helminths in School Children [NCT01379326]Phase 4250 participants (Actual)Interventional2011-12-31Completed
Double-Blind, Placebo-Controlled, Randomized, Prospective, Two-Stage, Two-Arm Study to Evaluate the Efficaciousness and Safety of a Double Treatment Plan Using a Combination of Mebendazole and Quinfamide for Treating Intestinal Helminthiasis and Amebiasis [NCT02385058]Phase 4100 participants (Actual)Interventional2005-10-31Completed
Improving Early Childhood Growth and Development in Resource-poor LMICs by Incorporating Deworming in Integrated Child Health Care [NCT01314937]Phase 41,760 participants (Anticipated)Interventional2011-09-30Completed
A Single-Dose, Open-Label, Randomized, 2-Way Crossover Study to Assess the Effect of Food on the Bioavailability of Mebendazole From a Fast-Disintegrating Chewable Formulation of Mebendazole in Healthy Subjects [NCT02051738]Phase 11 participants (Actual)Interventional2014-02-28Completed
A Phase I Study of Mebendazole for the Treatment of Pediatric Gliomas [NCT01837862]Phase 1/Phase 236 participants (Anticipated)Interventional2013-10-22Recruiting
An Open-Label, Single-Dose Study to Assess the Safety of 500-mg Mebendazole Chewable Formulation in Children 2 to 10 Years of Age, Inclusive [NCT01173562]Phase 3397 participants (Actual)Interventional2010-02-28Completed
Efficacy and Safety of a Single-dose Regimen and a Multi-dose Regimen of Mebendazole Against Hookworm Infections in Children and Adolescents in Ghana: a Randomized Controlled Trial [NCT03261596]Phase 40 participants (Actual)Interventional2017-09-30Withdrawn(stopped due to In light of new evidence, the decision was made by the sponsor to not proceed.)
A Study on the Effectiveness of IFA Supplementation, Deworming, and Nutrition Education in Addressing Anemia Among Adolescent Girls in Two Counties in Liberia [NCT05073562]0 participants (Actual)Interventional2021-10-31Withdrawn(stopped due to Change in funding availability)
The Efficacy of 5 Anthelmintic Regimes Against T. Trichiura Infections in Schoolchildren in Jimma, Ethiopia [NCT01327469]Phase 42,250 participants (Actual)Interventional2010-12-31Completed
Gaps in Helminth Control: Safety and Efficacy of Drug Combinations. Praziquantel Study [NCT01050374]650 participants (Anticipated)Interventional2007-10-31Completed
Gaps in Helminth Control: Safety and Efficacy of Drug Combinations. Study on Trichuris Trichiura. [NCT01050452]750 participants (Anticipated)Interventional2007-10-31Completed
Phase I Study of Mebendazole Therapy for Recurrent/Progressive Pediatric Brain Tumors [NCT02644291]Phase 116 participants (Actual)Interventional2016-05-31Completed
RDD1609 as a Treatment for Idiopathic Pruritus Ani: A Randomized Double Blinded Placebo Controlled Crossover Study [NCT03757403]Phase 20 participants (Actual)Interventional2020-05-01Withdrawn(stopped due to Covid-19)
Phase I Study of Mebendazole in Newly Diagnosed High-Grade Glioma Patients Receiving Temozolomide [NCT01729260]Phase 124 participants (Actual)Interventional2013-04-04Completed
Different Drug Combinations Against Hookworm Infection in School-aged Children in the Lao People's Democratic Republic, a Single Blind, Randomised Controlled Trial [NCT03278431]Phase 4420 participants (Actual)Interventional2017-09-27Completed
Evaluation of Anthelminthics and Multivitamins for Treatment of Severe Anemia in Pregnant Women and Children 6-24 Months of Age in Pakistan [NCT00116493]Phase 31,009 participants (Actual)Interventional2004-04-30Completed
Comparative Efficacy of Different Mebendazole Polymorphs in the Treatment of Soil-transmitted Helminth Infections [NCT01350271]Phase 3214 participants (Actual)Interventional2011-05-31Completed
Phase 2 Study of Avapritinib in Patients With CKIT or PDGFRA Mutation-Positive Malignant Solid Tumors [NCT04771520]Phase 250 participants (Anticipated)Interventional2021-01-20Recruiting
Optimization of Mass Drug Administration With Existing Drug Regimens for Lymphatic Filariasis and Onchocerciasis [NCT01905423]17,108 participants (Actual)Observational2011-05-31Completed
Efficacy and Safety of a New Chewable Tablet of Mebendazole Versus the Swallowable, Standard Tablet of Mebendazole Against Hookworm Infections in Children: a Randomized Controlled Trial [NCT03995680]Phase 2397 participants (Actual)Interventional2019-07-12Completed
A Double-Blind, Randomized, Multi-Center, Parallel-Group, Placebo-Controlled Study to Evaluate the Efficacy and Safety of a Single Dose of a 500-mg Chewable Tablet of Mebendazole in the Treatment of Soil-Transmitted Helminth Infections (Ascaris Lumbricoid [NCT02034162]Phase 3295 participants (Actual)Interventional2014-12-31Completed
A Phase I Study of [18F]DASA-23 as a PET Tracer for Evaluating Pyruvate Kinase M2 (PKM2) Expression in Healthy Volunteers and in Patients With Intracranial Tumors [NCT03539731]Phase 127 participants (Actual)Interventional2018-04-23Active, not recruiting
Preventing Unnecessary Blood Transfusions in Pregnant Women in Africa Through Effective Primary Health Care [NCT00148629]Phase 32,500 participants Interventional2004-04-30Active, not recruiting
To Study the Effects of Addition of Mebendazole to Lenvatinib in Cirrhotics With Advanced Hepatocellular Carcinoma. [NCT04443049]170 participants (Anticipated)Interventional2020-07-10Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT01350271 (3) [back to overview]Faecal Egg Count Reduction 1 (FECR1)
NCT01350271 (3) [back to overview]Faecal Egg Count Reduction 2 (FECR2)
NCT01350271 (3) [back to overview]Cure Rate
NCT01905423 (6) [back to overview]Prevalence of Ascaris Infection
NCT01905423 (6) [back to overview]Prevalence of Circulating Filarial Antigen in Blood as Determined by ICT Card Test
NCT01905423 (6) [back to overview]Prevalence of Hookworm Infection
NCT01905423 (6) [back to overview]Prevalence of Microfilaria in Blood as Determined by Microscopy of Participant Blood
NCT01905423 (6) [back to overview]Prevalence of Positive Brugia Rapid Antifilarial Antibody Tests
NCT01905423 (6) [back to overview]Prevalence of Trichuris Infection
NCT02034162 (10) [back to overview]Time to Reach Maximum Plasma Concentration (Tmax) of Mebendazole
NCT02034162 (10) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 to 8 Hours (AUC8h) of Mebendazole
NCT02034162 (10) [back to overview]Area Under the Plasma Concentration-Time Curve From Time Zero to Time of the Last Quantifiable Concentration AUC(0-last) of Mebendazole
NCT02034162 (10) [back to overview]Cure Rate for Ascaris Lumbricoides at the End of Double-blind Treatment Period
NCT02034162 (10) [back to overview]Cure Rate for Trichuris Trichiura at the End of Double-blind Treatment Period
NCT02034162 (10) [back to overview]Egg Count Reduction Rate (Percent) for Ascaris Lumbricoides Infestation at the End of Double-blind Treatment Period
NCT02034162 (10) [back to overview]Egg Count Reduction Rate (Percent) for Trichuris Trichiura Infestation at the End of Double-blind Treatment Period
NCT02034162 (10) [back to overview]Maximum Plasma Concentration (Cmax) of Mebendazole
NCT02034162 (10) [back to overview]Number of Participants Reporting Treatment Emergent Adverse Event (TEAE) in Double-Blind Treatment Period
NCT02034162 (10) [back to overview]Number of Participants Reporting Treatment Emergent Adverse Event (TEAE) in Open-Label Treatment Period
NCT03245398 (9) [back to overview]Arithmetic ERR of Both Mebendazole Regimens Against Trichuris Trichiura
NCT03245398 (9) [back to overview]Arithmetic ERR of the Two Regimens of Mebendazole Against Hookworm
NCT03245398 (9) [back to overview]CR of Both Mebendazole Regimens Against Trichuris Trichiura
NCT03245398 (9) [back to overview]Cure Rate (CR) of Both Mebendazole Regimens Against Ascaris Lumbricoides
NCT03245398 (9) [back to overview]Cure Rate (CR) of Mebendazole Against Hookworm
NCT03245398 (9) [back to overview]Geometric ERR of Both Mebendazole Regimens Against Ascaris Lumbricoides.
NCT03245398 (9) [back to overview]Geometric ERR of Both Mebendazole Regimens Against Trichuris Trichiura
NCT03245398 (9) [back to overview]Geometric Mean Egg Reduction Rate (ERR) of the Two Regimens of Mebendazole Against Hookworm
NCT03245398 (9) [back to overview]Arithmetic ERR of Both Mebendazole Regimens Against Ascaris Lumbricoides
NCT03995680 (9) [back to overview]Arithmetic ERR of the Two Formulations of Mebendazole Against Hookworm
NCT03995680 (9) [back to overview]CR of Both Mebendazole Formulations Against Ascaris Lumbricoides
NCT03995680 (9) [back to overview]CR of Both Mebendazole Regimens Against Trichuris Trichiura
NCT03995680 (9) [back to overview]Cure Rate (CR) of Mebendazole Against Hookworm
NCT03995680 (9) [back to overview]Geometric ERR of Both Mebendazole Formulations Against Ascaris Lumbricoides.
NCT03995680 (9) [back to overview]Geometric ERR of Both Mebendazole Formulations Against Trichuris Trichiura
NCT03995680 (9) [back to overview]Geometric Mean Egg Reduction Rate (ERR) of the Two Formulations of Mebendazole Against Hookworm
NCT03995680 (9) [back to overview]Arithmetic ERR of Both Mebendazole Formulations Against Trichuris Trichiura
NCT03995680 (9) [back to overview]Arithmetic ERR of Both Mebendazole Formulations Against Ascaris Lumbricoides

Faecal Egg Count Reduction 1 (FECR1)

FECR1= {[(Arithmetic mean of pretreatment egg counts)-(arithmetic mean of posttreatment egg counts)]÷(arithmetic mean of pretreatment egg counts)}×100 (NCT01350271)
Timeframe: Two weeks

Interventionpercentage of eggs excreted (Number)
Placebo-6.6
Mebendazole Polymorph A and C 500 mg86.1
Mebendazole Polymorph C 500 mg84.5

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Faecal Egg Count Reduction 2 (FECR2)

FECR2=〈Arithmetic mean {[(pretreatment egg count)-(posttreatment egg count)]÷(pretreatment egg count)}〉×100 (NCT01350271)
Timeframe: Two weeks

Interventionpercentage of eggs excreted (Mean)
Placebo-108.1
Mebendazole Polymorph A and C 500 mg66.2
Mebendazole Polymorph C 500 mg49.8

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Cure Rate

Cure rate={(Number positive pretreatment - Number positive posttreatment)÷(Number positive pretreatment)}×100 (NCT01350271)
Timeframe: Two weeks

Interventionpercentage of participants (Number)
Placebo16.3
Mebendazole Polymorph A and C 500 mg28.3
Mebendazole Polymorph C 500 mg18.8

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Prevalence of Ascaris Infection

Prevalence of Ascaris infection is defined by the number of participants with any Ascaris worm eggs present in their stool sample as analyzed with microscopy. (NCT01905423)
Timeframe: 2 Years

,,,,
InterventionParticipants (Count of Participants)
BaselineYear 1Year 2
Lewomada (1x Annual MDA)561718
Paga (1x Annual MDA)88135107
Pekalongan (1x Annual MDA)19110
Pekalongan (2x Annual MDA)5860
Pruda (2x Annual MDA)3473

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Prevalence of Circulating Filarial Antigen in Blood as Determined by ICT Card Test

"Prevalence of filarial antigenemia (detected with the Binax Filariasis Now card test ICT card test) among the population surveyed. Prevalence data are expressed as %." (NCT01905423)
Timeframe: 3 years

,,,,
InterventionParticipants (Count of Participants)
BaselineYear 1Year 2Year 3
Lewomada (1x Annual MDA)47121336
Paga (1x Annual MDA)14020
Pekalongan (1x Annual MDA)1185100
Pekalongan (2x Annual MDA)1026300
Pruda (2x Annual MDA)2359110672

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Prevalence of Hookworm Infection

Prevalence of hookworm infection is defined by the number of participants with any hookworm eggs present in their stool sample as analyzed with microscopy. (NCT01905423)
Timeframe: 2 years

,,,,
InterventionParticipants (Count of Participants)
BaselineYear 1Year 2
Lewomada (1x Annual MDA)22611897
Paga (1x Annual MDA)2511865
Pekalongan (1x Annual MDA)000
Pekalongan (2x Annual MDA)000
Pruda (2x Annual MDA)359087

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Prevalence of Microfilaria in Blood as Determined by Microscopy of Participant Blood

Microfilariae (filarial parasites) will be detected in blood smears by microscopy. Samples will be collected in annual and semiannual community surveys. Prevalence rates (a measure of the disease rates in the population sampled) are expressed as % positive for microfilaremia (having microfilaria in the blood). (NCT01905423)
Timeframe: 3 years

,,,,
InterventionParticipants (Count of Participants)
Baseline (pre-MDA)Year 1Year 2Year 3
Lewomada (1x Annual MDA)36963
Paga (1x Annual MDA)541160
Pekalongan (1x Annual MDA)462800
Pekalongan (2x Annual MDA)453000
Pruda (2x Annual MDA)146371512

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Prevalence of Positive Brugia Rapid Antifilarial Antibody Tests

This outcome is reported as the frequency of participants with positive Brugia Rapid antifilarial antibody tests. Data was only collected at baseline and at year 3 for this outcome measure and no antibody data was collected for the Pekalongan study sites. (NCT01905423)
Timeframe: 3 years

,,,,
InterventionParticipants (Count of Participants)
BaselineYear 1Year 2Year 3
Lewomada (1x Annual MDA)22916813436
Paga (1x Annual MDA)1750016
Pekalongan (1x Annual MDA)0000
Pekalongan (2x Annual MDA)0000
Pruda (2x Annual MDA)2970037

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Prevalence of Trichuris Infection

Prevalence of trichuris infection is defined by the number of participants with any trichuris worm eggs present in their stool sample as analyzed with microscopy. (NCT01905423)
Timeframe: 2 years

,,,,
InterventionParticipants (Count of Participants)
BaselineYear 1Year 2
Lewomada (1x Annual MDA)452523
Paga (1x Annual MDA)689384
Pekalongan (1x Annual MDA)120350
Pekalongan (2x Annual MDA)352650
Pruda (2x Annual MDA)8813

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Time to Reach Maximum Plasma Concentration (Tmax) of Mebendazole

The Time to Reach Maximum Plasma Concentration (Tmax) is time to reach the maximum plasma concentration. (NCT02034162)
Timeframe: Predose, 1, 2, 3, 5, 8 and 24 hours postdose at visit 4 (Day 20; 1 day after Visit 3)

Interventionhours (Mean)
Mebendazole: Group 1 (1 to <3 Years)2.5
Mebendazole: Group 2 (3 to 6 Years)2
Mebendazole: Group 3 (7 to 16 Years)3

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Area Under the Plasma Concentration-time Curve From Time 0 to 8 Hours (AUC8h) of Mebendazole

The (AUC8h) is the area under the plasma concentration-time curve from time 0 to 8 hours Post-dose. (NCT02034162)
Timeframe: Predose, 1, 2, 3, 5, 8 and 24 hours postdose at visit 4 (Day 20; 1 day after Visit 3)

Interventionnanogram hour per Milliliters(ng*h/mL) (Mean)
Mebendazole: Group 1 (1 to <3 Years)697
Mebendazole: Group 2 (3 to 6 Years)242
Mebendazole: Group 3 (7 to 16 Years)182

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Area Under the Plasma Concentration-Time Curve From Time Zero to Time of the Last Quantifiable Concentration AUC(0-last) of Mebendazole

The (AUC [0-last]) is the area under the plasma concentration-time curve from time 0 to time of the last quantifiable concentration. (NCT02034162)
Timeframe: Predose, 1, 2, 3, 5, 8 and 24 hours postdose at visit 4 (Day 20; 1 day after Visit 3)

Interventionng*h/mL (Mean)
Mebendazole: Group 1 (1 to <3 Years)1320
Mebendazole: Group 2 (3 to 6 Years)416
Mebendazole: Group 3 (7 to 16 Years)387

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Cure Rate for Ascaris Lumbricoides at the End of Double-blind Treatment Period

Cure is defined as a post-treatment egg count of zero in participants who had a positive egg count at baseline. (NCT02034162)
Timeframe: At Visit 3 (Day 19) of Double-blind treatment period

Interventionpercentage of participants (Number)
Double-blind Placebo11.1
Double-blind Mebendazole 500 mg83.7

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Cure Rate for Trichuris Trichiura at the End of Double-blind Treatment Period

Cure is defined as a post-treatment egg count of zero in participants who had a positive egg count at baseline. (NCT02034162)
Timeframe: At Visit 3 (Day 19) of Double-blind treatment period

Interventionpercentage of participants (Number)
Double-blind Placebo7.6
Double-blind Mebendazole 500 mg33.9

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Egg Count Reduction Rate (Percent) for Ascaris Lumbricoides Infestation at the End of Double-blind Treatment Period

Percent egg count reduction is calculated as average egg count at end of treatment period of a treatment group minus average egg count at baseline of the treatment group divided by average egg count at baseline of the treatment group. (NCT02034162)
Timeframe: Baseline and Day 19 (Visit 3) at the End of Double-blind Treatment Period

Interventionpercent change in egg count (Number)
Double-blind Placebo-19.2
Double-blind Mebendazole 500 mg-97.9

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Egg Count Reduction Rate (Percent) for Trichuris Trichiura Infestation at the End of Double-blind Treatment Period

Percent egg count reduction is calculated as average egg count at end of treatment period of a treatment group minus average egg count at baseline of the treatment group divided by average egg count at baseline of the treatment group. (NCT02034162)
Timeframe: Baseline and Day 19 (Visit 3) at the End of Double-blind Treatment Period

Interventionpercent change in egg count (Number)
Double-blind Placebo-10.5
Double-blind Mebendazole 500 mg-59.7

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Maximum Plasma Concentration (Cmax) of Mebendazole

The Cmax is the maximum plasma concentration. (NCT02034162)
Timeframe: Predose, 1, 2, 3, 5, 8 and 24 hours postdose at visit 4 (Day 20; 1 day after Visit 3)

Interventionnanogram per Milliliters (ng/mL) (Mean)
Mebendazole: Group 1 (1 to <3 Years)210.0
Mebendazole: Group 2 (3 to 6 Years)49.9
Mebendazole: Group 3 (7 to 16 Years)34.2

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Number of Participants Reporting Treatment Emergent Adverse Event (TEAE) in Double-Blind Treatment Period

An AE is any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. A serious adverse event (SAE) is an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. (NCT02034162)
Timeframe: Up to Visit 3 (Day 19 +/-2)

Interventionparticipants (Number)
Double-blind Placebo8
Double-blind Mebendazole 500 mg9

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Number of Participants Reporting Treatment Emergent Adverse Event (TEAE) in Open-Label Treatment Period

An AE is any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. A serious adverse event (SAE) is an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. (NCT02034162)
Timeframe: At Visit 3 (Day 19+/-2) followed up to Visit 5 (Day 7+/-1 from Visit 3)

Interventionparticipants (Number)
Open-label Mebendazole 500 mg7

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Arithmetic ERR of Both Mebendazole Regimens Against Trichuris Trichiura

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(arithmetic mean EPG at follow-up/arithmetic mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (arithmetic mean at follow-up/arithmetic mean at baseline)*100)." (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage change (Mean)
Single 500 mg Dose of Mebendazole-49.1
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole-91.6

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Arithmetic ERR of the Two Regimens of Mebendazole Against Hookworm

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(arithmetic mean EPG at follow-up/arithmetic mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (arithmetic mean at follow-up/arithmetic mean at baseline)*100)." (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage change (Mean)
Single Dose of Mebendazole-52.7
Multiple Dose of Mebendazole-99.8

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CR of Both Mebendazole Regimens Against Trichuris Trichiura

Cure rates (CRs) will be calculated as the percentage of egg-positive participants at baseline who become egg-negative after treatment. (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage of participants cured (Number)
Single 500 mg Dose of Mebendazole6.8
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole42.9

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Cure Rate (CR) of Both Mebendazole Regimens Against Ascaris Lumbricoides

Cure rates (CRs) will be calculated as the percentage of egg-positive participants at baseline who become egg-negative after treatment. (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage of participants cured (Number)
Single 500 mg Dose of Mebendazole100
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole98

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Cure Rate (CR) of Mebendazole Against Hookworm

Cure rates (CRs) will be calculated as the percentage of egg-positive participants at baseline who become egg-negative after treatment. (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage of participants cured (Number)
Single 500 mg Dose of Mebendazole13
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole97.9

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Geometric ERR of Both Mebendazole Regimens Against Ascaris Lumbricoides.

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(geometric mean EPG at follow-up/geometric mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (geometric mean at follow-up/geometric mean at baseline)*100)." (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage change (Mean)
Single 500 mg Dose of Mebendazole-100
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole-100

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Geometric ERR of Both Mebendazole Regimens Against Trichuris Trichiura

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(geometric mean EPG at follow-up/geometric mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (geometric mean at follow-up/geometric mean at baseline)*100)." (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage of change (Mean)
Single 500 mg Dose of Mebendazole-71.7
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole-98.1

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Geometric Mean Egg Reduction Rate (ERR) of the Two Regimens of Mebendazole Against Hookworm

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(geometric mean EPG at follow-up/geometric mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (geometric mean at follow-up/geometric mean at baseline)*100)." (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage change (Geometric Mean)
Single 500 mg Dose of Mebendazole-68.0
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole-100

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Arithmetic ERR of Both Mebendazole Regimens Against Ascaris Lumbricoides

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(arithmetic mean EPG at follow-up/arithmetic mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (arithmetic mean at follow-up/arithmetic mean at baseline)*100)." (NCT03245398)
Timeframe: baseline (before treatment) and 18 to 22 days post-treatment

Interventionpercentage change (Mean)
Single 500 mg Dose of Mebendazole-100
Multiple (Bid for 3 Days) Dose of 100 mg Mebendazole-99.1

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Arithmetic ERR of the Two Formulations of Mebendazole Against Hookworm

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(arithmetic mean EPG at follow-up/arithmetic mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (arithmetic mean at follow-up/arithmetic mean at baseline)*100)." (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage change in hookworm egg counts (Number)
Chewable Tablet of Mebendazole38.2
Swallowable Tablet of Mebendazole28.1

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CR of Both Mebendazole Formulations Against Ascaris Lumbricoides

Cure rates (CRs) will be calculated as the percentage of egg-positive participants at baseline who become egg-negative after treatment. (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage of participants (Number)
Chewable Tablet of Mebendazole95.3
Swallowable Tablet of Mebendazole97.8

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CR of Both Mebendazole Regimens Against Trichuris Trichiura

Cure rates (CRs) will be calculated as the percentage of egg-positive participants at baseline who become egg-negative after treatment. (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage of participants (Number)
Chewable Tablet of Mebendazole9.8
Swallowable Tablet of Mebendazole7.3

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Cure Rate (CR) of Mebendazole Against Hookworm

Cure rates (CRs) will be calculated as the percentage of egg-positive participants at baseline who become egg-negative after treatment. (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage of participants (Number)
Chewable Tablet of Mebendazole12.7
Swallowable Tablet of Mebendazole11.2

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Geometric ERR of Both Mebendazole Formulations Against Ascaris Lumbricoides.

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(geometric mean EPG at follow-up/geometric mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (geometric mean at follow-up/geometric mean at baseline)*100)." (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage change in A. lumbr egg counts (Number)
Chewable Tablet of Mebendazole99.9
Swallowable Tablet of Mebendazole99.9

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Geometric ERR of Both Mebendazole Formulations Against Trichuris Trichiura

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(geometric mean EPG at follow-up/geometric mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (geometric mean at follow-up/geometric mean at baseline)*100)." (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage change in T. trich egg counts (Number)
Chewable Tablet of Mebendazole73.3
Swallowable Tablet of Mebendazole74.2

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Geometric Mean Egg Reduction Rate (ERR) of the Two Formulations of Mebendazole Against Hookworm

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(geometric mean EPG at follow-up/geometric mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (geometric mean at follow-up/geometric mean at baseline)*100)." (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage change in hookworm egg counts (Number)
Chewable Tablet of Mebendazole68.5
Swallowable Tablet of Mebendazole70.8

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Arithmetic ERR of Both Mebendazole Formulations Against Trichuris Trichiura

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(arithmetic mean EPG at follow-up/arithmetic mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (arithmetic mean at follow-up/arithmetic mean at baseline)*100)." (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage change in T. trich egg counts (Number)
Chewable Tablet of Mebendazole52.9
Swallowable Tablet of Mebendazole50.9

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Arithmetic ERR of Both Mebendazole Formulations Against Ascaris Lumbricoides

"Eggs per gram of stool (EPG) will be assessed by adding up the egg counts from the quadruplicate Kato-Katz thick smears and multiplying this number by a factor of six. The egg reduction rate (ERR) is calculated as follows: ERR = (1-(arithmetic mean EPG at follow-up/arithmetic mean EPG at baseline))*100). Note: in contrast to the publication the outcome measure entry mask requires the complementary percentage: (arithmetic mean at follow-up/arithmetic mean at baseline)*100)." (NCT03995680)
Timeframe: Baseline (before treatment) and sometime between 14 and 21 days post-treatment

Interventionpercentage change in A. lumbr egg counts (Number)
Chewable Tablet of Mebendazole98.7
Swallowable Tablet of Mebendazole99.8

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