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dithiothreitol

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Description

Dithiothreitol (DTT) is a small-molecule reducing agent commonly used in biochemistry and molecular biology. It is a white crystalline solid that is soluble in water and other polar solvents. DTT is synthesized through a reaction of 2,3-dimercaptopropanol with formaldehyde. DTT works by reducing disulfide bonds in proteins, which can be important for a variety of reasons. For example, disulfide bonds can help to stabilize the structure of proteins, and they can also play a role in protein folding. By reducing disulfide bonds, DTT can help to denature proteins, which can be useful for studying protein structure and function. DTT is widely used in research as a reducing agent in various applications. For example, DTT is used to reduce disulfide bonds in proteins, which can help to denature the proteins and make them more soluble. It is also used in protein purification, where it can be used to reduce disulfide bonds in proteins that are bound to a solid support. DTT is also commonly used to break disulfide bonds in proteins before SDS-PAGE, a technique for separating proteins based on their size. This helps to ensure that the proteins are unfolded and can be separated according to their size. DTT is important because it allows researchers to study proteins in a more controlled environment. By reducing disulfide bonds, DTT can help to denature proteins, which can be useful for studying protein structure and function. DTT is studied because it is an important tool for research in biochemistry and molecular biology.'

1,4-dimercaptobutane-2,3-diol : A glycol that is butane-2,3-diol in which a hydrogen from each of the methyl groups is replaced by a thiol group. [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]

1,4-dithiothreitol : The threo-diastereomer of 1,4-dimercaptobutane-2,3-diol. [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]

Cross-References

ID SourceID
PubMed CID19001
CHEMBL ID47903
CHEBI ID25189
CHEBI ID18320
SCHEMBL ID87345
MeSH IDM0006621
PubMed CID439196
CHEMBL ID406270
CHEBI ID42106
SCHEMBL ID538995
MeSH IDM0006621

Synonyms (127)

Synonym
1,4-bissulfanylbutane-2,3-diol
1,4-dimercapto-2,3-butanediol
7634-42-6
1,4-dimercaptobutane-2,3-diol
CHEBI:25189
1,4-disulfanylbutane-2,3-diol
LS-13012
2,3-butanediol, 1,4-dimercapto-, d-threo-
inchi=1/c4h10o2s2/c5-3(1-7)4(6)2-8/h3-8h,1-2h
threitol, 1,4-dithio-, dl-
dithiotreitol
DTT ,
dl-theo-1,4-dimercapto-2,3-butanediol
1,4-bis(sulfanyl)butane-2,3-diol
2,3-butanediol, 1,4-dimercapto-
1,4-dithio-dl-threitol
cleland's reagent
dl-dithiothreitol
sputolysin
2,3-butanediol, 1,4-dimercapto-, (r*,r*)-
rac-dithiothreitol
wr 34678
dithiothreitol ,
1,4-dithiothreitol
3483-12-3
D1071
27565-41-9
clelands reagent
D-8100
D-8200
D-8220
CHEBI:18320 ,
rel-(2r,3r)-1,4-disulfanylbutane-2,3-diol
(r*,r*)-1,4-dimercapto-2,3-butanediol
dl-1,4-dimercapto-2,3-butanediol
dl-2,3-dihydroxy-1,4-butanedithiol
dl-dtt
D3647
CHEMBL47903
AKOS004910031
A822424
einecs 231-563-2
FT-0606884
FT-0606912
FT-0606913
FT-0602264
2,3-butanediol,1,4-dimercapto-
BRD-A30142024-001-01-1
CCG-208027
SCHEMBL87345
d,l-dithiothreitol
(.+/-.)-dithiothreitol
2,3-butanediol, 1,4-dimercapto-, (r*,r*)-(.+/-.)-
2,3-butanediol, 1,4-dimercapto-, dl, threo-
1,4-disulfanyl-2,3-butanediol, dl, threo-
1,4-dithio-2,3-butanediol
STL451520
cleland's reagent;dte
cleland's reagent;dtt;dithiothreitol
BCP24764
DTXSID80859811
Q28529689
2,3-butanediol, 1,4-dimercapto-(r*,r*)-()-or,dithiothreitol
BCP34516
1,4-dithio-dl-threitol;dl-1,4-dithiothreitol;dl-dithiothreitol
SB45080
EN300-95414
(r*,r*)-1,4-dimercaptobutane-2,3-diol
2,3-butanediol, 1,4-dimercapto-, (2r,3r)-rel-
2,3-butanediol, 1,4-dimercapto-, (theta,theta)-(+/-)-
(r*,r*)-(+-)-1,4-dimercapto-2,3-butanediol
(r*,r*)-(1)-1,4-dimercaptobutane-2,3-diol
threitol, 1,4-dithio-
cleland reagent
einecs 222-468-7
2,3-butanediol, 1,4-dimercapto-, (r*,r*)- (+-)-
ai3-62064
brn 1719757
ccris 3617
einecs 248-531-9
2,3-butanediol, 1,4-dimercapto-, dl-threo-
2,3-dihydroxy-1,4-dithiobutane
C00265
dl-threo-1,4-dimercapto-2,3-butanediol
l-(-)-dithiothreitol, >=95%
l-dithiothreitol
(2r,3r)-1,4-disulfanylbutane-2,3-diol
l-threo-1,4-dimercapto-2,3-butanediol
(2r,3r)-1,4-dimercaptobutane-2,3-diol
l-1,4-dithiothreitol
16096-97-2
l-dtt
CHEBI:42106 ,
DB04447
l-1,4-disulfanylbutane-2,3-diol
threitol, dithio-
23968FDA-4EA3-46CD-8871-0DEB9D9EA0B8
CHEMBL406270
(2r,3r)-1,4-bis(sulfanyl)butane-2,3-diol
l-cleland's reagent
(2r,3r)-(-)-2,3-dihydroxy-1,4-butanedithiol
D1589
(2r,3r)-(-)-1,4-dimercapto-2,3-butanediol
hsdb 8422
t8id5yzu6y ,
3-01-00-02360 (beilstein handbook reference)
unii-t8id5yzu6y
l-(-)-dithiothreitol
1,4-dimercapto-2,3-butanediol, dl-
dithiothreitol [inci]
wr-34678
cleland reagent racemic
1,4-dithiothreitol [mi]
2,3-butanediol, 1,4-dimercapto-, (r*,r*)- (+/-)-
S6829
HY-15917
SCHEMBL538995
(-)-1,4-dithio-l-threitol
mfcd00064305
AKOS028109573
AS-64942
D70251
ldtt
(2r,3r)-rel-1,4-dimercapto-2,3-butanediol
Q27104490
T70362
DTXSID501316708

Research Excerpts

Overview

1,4-Dithiothreitol (DTT) is an important small-molecular reducing agent and has extensive applications in biochemistry, peptide/protein chemistry and clinical medicine. It contributes significantly to the folding process of proteins and maintaining endoplasmic reticulum (ER) homeostasis.

ExcerptReferenceRelevance
"1,4-Dithiothreitol (DTT) is a robust reducing agent that contributes significantly to the folding process of proteins and maintaining endoplasmic reticulum (ER) homeostasis. "( The development of an endoplasmic reticulum-targeting fluorescent probe for the imaging of 1,4-dithiothreitol (DTT) in living cells.
Dong, B; Lin, W; Lu, Y; Mehmood, AH; Song, W; Sun, Y, 2021
)
1.4
"1,4-Dithiothreitol (DTT) is an important small-molecular reducing agent and has extensive applications in biochemistry, peptide/protein chemistry and clinical medicine. "( Two-photon imaging of 1,4-dithiothreitol (DTT) by a red-emissive fluorescent probe in living cells, tissues and animals.
Dong, B; Kong, X; Lin, W; Song, W; Wang, C; Zhang, N, 2018
)
1.34
"Dithiothreitol is a chemical reagent with a wide actuation spectrum not only from a laboratorial view but also from a therapeutic standpoint, more clinical and practical."( Dithiothreitol revisited in red cells: a new head for an old hat.
Lopes de Almeida, JP; Saldanha, C, 2010
)
2.52
"Dithiothreitol (DTT) is a reductant commonly used to reduce and unfold disulfide-stabilized lysozymes."( Refolding of partially and fully denatured lysozymes.
Hsieh, HJ; Lin, JL; Ruaan, RC, 2007
)
1.06
"Dithiothreitol (DTT) is a well-known dithiol agent reported to modulate the action of ATO."( Dithiothreitol abrogates the effect of arsenic trioxide on normal rat liver mitochondria and human hepatocellular carcinoma cells.
Kumar, R; Mukhopadhyay, AK; Paul, MK, 2008
)
2.51
"Dithiothreitol (DTT) is a sulfhydryl reducing agent used as a radioprotectant. "( Dithiothreitol elicits epileptiform activity in CA1 of the guinea pig hippocampal slice.
Pellmar, TC; Tolliver, JM, 1987
)
3.16

Effects

Dithiothreitol (2 mM) has a large stabilizing effect on the binding capacity at 0 degrees C but only a small effect at 25 degrees C. It has a marked stimulatory effect on the rate of conversion.

Dithiothreitol (DTT) has wide applications in cell biology and biochemistry. It has been proposed as an alternative treatment to sonication for microbiological diagnosis of prosthetic joint infections. DithiOTHreitol has a marked stimulatory effect on the rate of conversion.

ExcerptReferenceRelevance
"Dithiothreitol (2 mM) has a large stabilizing effect on the binding capacity at 0 degrees C but only a small effect at 25 degrees C."( Activation of thymocyte glucocorticoid receptors to the steroid binding form. The roles of reduction agents, ATP, and heat-stable factors.
Hammond, ND; Pratt, WB; Sando, JJ; Stratford, CA, 1979
)
0.98
"Dithiothreitol has a marked stimulatory effect on the rate of conversion."( Effect of cortisol on the in vitro hepatic conversion of thyroxine to triiodothyronine in brook charr (Salvelinus fontinalis Mitchill).
Flett, PA; Leatherland, JF; Vijayan, MM, 1988
)
1
"DL-dithiothreitol has been described as a valid method for biofilm detachment on orthopedic devices."( Unexpected Listeria monocytogenes detection with a dithiothreitol-based device during an aseptic hip revision.
Allizond, V; Banche, G; Bistolfi, A; Cuffini, AM; Galletta, C; Iannantuoni, MR; Marra, ES; Massè, A; Merlino, C, 2018
)
1.25
"1,4-Dithiothreitol (DTT) has wide applications in cell biology and biochemistry. "( A new xanthene-based two-photon fluorescent probe for the imaging of 1,4-dithiothreitol (DTT) in living cells.
Dong, B; Kong, X; Lin, W; Song, W; Wang, C; Zhang, N, 2018
)
1.27
"Dithiothreitol (DTT) has been proposed as an alternative treatment to sonication for microbiological diagnosis of prosthetic joint infections."( Treatment With Dithiothreitol Improves Bacterial Recovery From Tissue Samples in Osteoarticular and Joint Infections.
Bortolin, M; De Vecchi, E; Drago, L; Romanò, CL; Signori, V, 2016
)
1.51
"Dithiothreitol has been used to stabilize the substrate and quinolones to complex the ferric."( A kinetic method amenable to automation for ceruloplasmin estimation with inexpensive and stable reagents.
Ambade, V; Somani, BL, 2007
)
1.78
"Dithiothreitol (DTT) has been found to destroy the integrity of the LW antigen. "( The effect of dithiothreitol on the LW antigen.
Holland, TI; Konigshaus, GJ,
)
1.93
"Dithiothreitol (2 mM) has a large stabilizing effect on the binding capacity at 0 degrees C but only a small effect at 25 degrees C."( Activation of thymocyte glucocorticoid receptors to the steroid binding form. The roles of reduction agents, ATP, and heat-stable factors.
Hammond, ND; Pratt, WB; Sando, JJ; Stratford, CA, 1979
)
0.98
"Dithiothreitol has no effect."( Modification of optical responses associated with the action potential of lobster giant axons.
Kaplan, MW; Klein, MP, 1975
)
0.98
"Dithiothreitol has a marked stimulatory effect on the rate of conversion."( Effect of cortisol on the in vitro hepatic conversion of thyroxine to triiodothyronine in brook charr (Salvelinus fontinalis Mitchill).
Flett, PA; Leatherland, JF; Vijayan, MM, 1988
)
1
"Dithiothreitol has been found to prevent strand break formation by reacting with H-adduct radicals of poly(U) with a rate constant of 5 X 10(6) M-1 s-1."( Rate and rate-determining step of hydrogen-atom-induced strand breakage in poly(U) in aqueous solution under anoxic conditions.
Bothe, E; Selbach, H,
)
0.85

Actions

Dithiothreitol did not inhibit the binding of the beta-adrenergic antagonist [3H]dihydroalprenolol to adipocytes. The ligand could protect the receptor from the effect of the reagent.

ExcerptReferenceRelevance
"Dithiothreitol did not inhibit the binding of the beta-adrenergic antagonist [3H]dihydroalprenolol to adipocytes."( Insulin-like effects of dithiothreitol on isolated rat adipocytes.
Goko, H; Kawamuro, A; Matsuoka, A; Takashima, S, 1981
)
1.29
"Dithiothreitol could regenerate the binding capacity and the ligand could protect the receptor from the effect of the reagent."( Functions of interleukin-8 are mediated through thiol group(s) of IL-8 receptor in human polymorphonuclear neutrophils. Effects of 5,5'-dithio-bis(2-nitrobenzoic acid) on IL-8 receptor.
Ali, E; Dutta, S; Samanta, AK, 1993
)
1.01
"Dithiothreitol did not increase the basal activity of CB from SQCLC and the lung which indicates that reversibly oxidized forms of CB do not accumulate in the tumors and the lungs."( Cathepsin B, thiols and cysteine protease inhibitors in squamous-cell lung cancer.
Cermák, J; Kárová, B; Krepela, E; Procházka, J; Roubková, H, 1997
)
1.02
"dithiothreitol) were able to suppress chemiluminescence formation."( Cumene hydroperoxide-induced chemiluminescence in human erythrocytes: effect of antioxidants and sulfhydryl compounds.
Emerk, K; Sabuncu, N; Yalçin, AS, 1992
)
1

Treatment

Dithiothreitol (DTT) treatment of angiotensin II (Ang II) type 2 (AT(2) receptor potentiates ligand binding, but the underlying mechanism is not known. DithiOTHreitol treatment caused the microvilli to become more irregular in shape and diameter than those of untreated eggs.

ExcerptReferenceRelevance
"Dithiothreitol pre-treatment led to a higher number of positive samples, compared to controls (27 vs 19), leading to a statistically significant increase in the sensitivity of the microbiological count examination from 54.3 to 77.1% and in colony-forming units count from 1884 ± 2.129 CFU/mL with saline pre-treatment to 20.442 ± 19.270 with DTT pre-treatment (P = 0.02)."( Dithiotreitol pre-treatment of synovial fluid samples improves microbiological counts in peri-prosthetic joint infection.
Drago, L; Erasmo, R; Fidanza, A; Giannetti, A; Mavrogenis, AF; Romanò, CL; Romanò, D, 2023
)
2.35
"Dithiothreitol (DTT) treatment of red blood cells (RBCs) negates this interference."( A newly devised flow cytometric antibody binding assay helps evaluation of dithiothreitol treatment for the inactivation of CD38 on red blood cells.
Fujihara, H; Furumaki, H; Ino, K; Ishizuka, K; Kawabata, K; Nemoto, N; Obata, Y; Ohto, H; Ozawa, A; Shibata, H; Shinba, T; Takeshita, A; Watanabe, H; Yamada, C, 2021
)
1.57
"Dithiothreitol (DTT) treatment has been proposed as an alternative to sonication to improve diagnosis, reduce costs, and improve reliability of the procedure, but its efficacy remains poorly characterized."( Is Treatment With Dithiothreitol More Effective Than Sonication for the Diagnosis of Prosthetic Joint Infection?
Bianchi, G; Cadossi, M; Donati, D; Fantini, M; Gamberini, S; Giannini, S; Marcacci, M; Maso, A; Naldi, S; Neri, MP; Pignatti, G; Sambri, A; Sambri, V; Storni, E; Tassinari, M; Torri, A; Zannoli, S, 2018
)
1.54
"Dithiothreitol (DTT) treatment of panel red blood cells (RBCs) abolishes DARA interference."( Extending shelf life of dithiothreitol-treated panel RBCs to 28 days.
Bargetzi, M; Mihm, B; Sigle, JP; Suna, R, 2018
)
1.51
"Dithiothreitol treatment with a ratio of 30:25 (red blood cells:dithiothreitol) showed the same degree of haemolysis as with untreated panel cells. "( Thirty-three-day storage of dithiothreitol-treated red blood cells used to eliminate daratumumab interference in serological testing.
Andersen, P; Lone Akhtar, N; Lorenzen, H; Nielsen, M; Svendsen, L, 2018
)
2.22
"Dithiothreitol treatment, which reduced the extracellular S-S bridge-forming cysteines of ABCG2, had no effect on transport function but caused a significant decrease in 5D3 binding."( Interaction with the 5D3 monoclonal antibody is regulated by intramolecular rearrangements but not by covalent dimer formation of the human ABCG2 multidrug transporter.
Dokholyan, NV; Goda, K; Hegedus, C; Hegedus, T; Laczkó, R; Litman, T; Ozvegy-Laczka, C; Sarkadi, B; Sorrentino, BP; Váradi, A; Várady, G, 2008
)
1.07
"Dithiothreitol treatment enhanced the binding of agonist ([125I]angiotensin II) and antagonist ([125I](Sar1,Ala8)-angiotensin II) to particulate and solubilized rat adrenal receptors, an effect attributable to inhibition of tracer degradation."( Solubilized adrenal angiotensin II receptors: studies on the site of action of sodium and calcium ions, and on the role of disulfide bridges.
Birabeau, MA; Capponi, AM; Vallotton, MB, 1984
)
0.99
"Dithiothreitol (DTT) treatment of WT or cyc- lymphoma membranes resulted in the simultaneous loss of epinephrine-stimulated adenylate cyclase activity and beta-adrenergic antagonist binding. "( Effect of dithiothreitol on the beta-adrenergic receptor of S49 wild type and cyc- lymphoma cells: decreased affinity of the ligand-receptor interaction.
Clark, RB; Green, DA; Rashidbaigi, A; Ruoho, A, 1983
)
2.11
"In dithiothreitol-treated cells, 125I-insulin binding was increased and this increase was accounted for by a change in affinity."( Insulin receptor regulation and desensitization in rat hepatoma cells. The loss of the oligomeric forms of the receptor correlates with the change in receptor affinity.
Crettaz, M; Jialal, I; Kahn, CR; Kasuga, M, 1984
)
0.78
"Dithiothreitol (DTT) treatment of control receptors prepared without iodoacetamide resulted in increased autophosphorylation."( Dithiothreitol stimulates insulin receptor autophosphorylation at the juxtamembrane domain.
Engl, J; Moule, M; Yip, CC, 1994
)
2.45
"When dithiothreitol-treated cells were extracted under nondenaturing conditions immunoprecipitates of newly synthesized albumin showed a complex polypeptide profile."( Dithiothreitol treatment induces heterotypic aggregation of newly synthesized secretory proteins in HepG2 cells.
Lukaczyk, T; Sawyer, JT; Yilla, M, 1994
)
2.19
"Dithiothreitol (DTT)-treatment of native EGZ showed that the disulphide bond was dispensable, both for catalysis and cellulose binding."( Periplasmic disulphide bond formation is essential for cellulase secretion by the plant pathogen Erwinia chrysanthemi.
Barras, F; Bortoli-German, I; Brun, E; Chippaux, M; Py, B, 1994
)
1.01
"Dithiothreitol treatment had little affect on [3H]AA release and metabolism but inhibited AA mass release."( Activation of cytosolic phospholipase A2 in permeabilized human neutrophils.
Bass, DA; Bauldry, SA; Wooten, RE, 1996
)
1.02
"Dithiothreitol treatment restored the sulfhydryl groups and enzyme activity."( Studies on identifying the catalytic role of Glu-204 in the active site of yeast invertase.
Maley, F; Reddy, A, 1996
)
1.02
"Dithiothreitol treatment destroyed all protective activity while bovine but not human albumin was partially inactivated by CNBr treatment."( Serum albumin is a specific inhibitor of apoptosis in human endothelial cells.
Beckmann, R; Bielek, E; Binder, BR; Fabry, A; Höfler, M; Hufnagl, P; Lockie, S; Vanyek, E; Wojta, J; Zoellner, H, 1996
)
1.02
"Upon dithiothreitol treatment, the 36-kDa species was diminished greatly or undetectable."( Evidence for a ninth gene, ptlI, in the locus encoding the pertussis toxin secretion system of Bordetella pertussis and formation of a PtlI-PtlF complex.
Burns, DL; Cafarella, TG; Farizo, KM, 1996
)
0.75
"Dithiothreitol-treatment of oxidized LDL, however, reduced the apoptotic activity by 76%."( Dehydroascorbic acid prevents apoptosis induced by oxidized low-density lipoprotein in human monocyte-derived macrophages.
Asmis, R; Wintergerst, ES, 1998
)
1.02
"Dithiothreitol (DTT) treatment of angiotensin II (Ang II) type 2 (AT(2)) receptor potentiates ligand binding, but the underlying mechanism is not known. "( Reversible inactivation of AT(2) angiotensin II receptor from cysteine-disulfide bond exchange.
Feng, YH; Karnik, SS; Saad, Y, 2000
)
1.75
"Dithiothreitol treatment also produced effects on secretion that were independent of nicotinic receptor activation."( Effects of sulfhydryl modification on adrenal nicotinic acetylcholine receptors: disulfide integrity is not essential for activation.
Free, RB; McKay, DB; Wenger, BW, 2000
)
1.03
"Dithiothreitol treatment of homogenates fully abolished the signals detected."( Detection, quantitation, purification, and identification of cardiac proteins S-thiolated during ischemia and reperfusion.
Byers, HL; Eaton, P; Leeds, N; Shattock, MJ; Ward, MA, 2002
)
1.04
"Dithiothreitol-treatment of intact cells induces the release of Uth1p, Sun4p and Sim1p from the cell wall."( Dual cell wall/mitochondria localization of the 'SUN' family proteins.
Boucheron, C; Camougrand, N; Manon, S; Velours, G, 2002
)
1.04
"Dithiothreitol treatment caused the microvilli to become more irregular in shape, length, and diameter than those of untreated eggs."( Changes in the topography of the sea urchin egg after fertilization.
Eddy, EM; Shapiro, BM, 1976
)
0.98
"Dithiothreitol (7.5 mM) treatment after preincubation with glucose fully restores the glucose-induced inhibition."( An oxidative mechanism is involved in high glucose-induced serum protein modification causing inhibition of endothelial cell proliferation.
Ito, H; Kawashima, S; Nakao-Hayashi, J, 1992
)
1
"Dithiothreitol treatment completely restores the active form."( Redox forms of human placenta glutathione transferase.
Barra, D; Caccuri, AM; Del Boccio, G; Federici, G; Lo Bello, M; Pennelli, A; Petruzzelli, R; Ricci, G, 1991
)
1
"Dithiothreitol treatment of ALR2 did not alter its properties toward other substrates or affect its inhibition by aldose reductase inhibitors such as sorbinil (2,4-dihydro-6-fluorospiro-[4H-1-benzopyran-4,4'-imidazolidine]-2' ,5'- dione), tolrestat (N-[[6-methoxy-5-(trifluoromethyl)-1-naphthalenyl]thioxomethyl]-N- methylglycine), or statil (3-[(4-bromo-2-fluorophenyl)methyl]-3,4-dihydro-4-oxo-1-phthalazineac etic acid)."( Aldehyde and aldose reductases from human placenta. Heterogeneous expression of multiple enzyme forms.
Deck, LM; Hunsaker, LA; Robinson, B; Stangebye, LA; Vander Jagt, DL, 1990
)
1
"The dithiothreitol-treated RuBisCO was activated by 12 mM NaHCO3 and 20 mM MgCl2, and the activated state was stable at least for 60 min in the presence of 4 mM ethylenediaminetetraacetate."( Characterization of ribulose 1,5-bisphosphate carboxylase/oxygenase from Euglena gracilis Z.
Harada, A; Kitaoka, S; Yokota, A, 1989
)
0.76
"Dithiothreitol treatment of adipocytes preferentially inactivated high-affinity binding sites."( Binding and structural properties of oxytocin receptors in isolated rat epididymal adipocytes.
Boland, D; Goren, HJ, 1987
)
0.99
"Pretreatment with dithiothreitol did not affect TH transport or its inhibition by pCMBS."( Importance of cysteine residues in the thyroid hormone transporter MCT8.
Groeneweg, S; Lima de Souza, EC; Peeters, RP; Visser, TJ; Visser, WE, 2013
)
0.71
"Pretreatment with dithiothreitol, an ERS stimulator mimicked the above cardioprotective effect."( Effect of sulfur dioxide preconditioning on rat myocardial ischemia/reperfusion injury by inducing endoplasmic reticulum stress.
Du, JB; Huang, XM; Jin, HF; Li, XY; Ochs, T; Tang, CS; Wang, XB, 2011
)
0.69
"Treatment with dithiothreitol restored modified MST to the original mass."( Post-translational regulation of mercaptopyruvate sulfurtransferase via a low redox potential cysteine-sulfenate in the maintenance of redox homeostasis.
Katayama, A; Nagahara, N, 2005
)
0.67
"Treatment with dithiothreitol removed as much as 80 to 85% of trypsinized virus particles incubated with human erythrocytes at 37 degrees C."( Attachment of Sendai virus particles to cell membranes: dissociation of adsorbed virus particles with dithiothreitol.
Beigel, M; Chejanovsky, N; Loyter, A, 1984
)
0.82
"Pretreatment with dithiothreitol and Pronase in the presence of EDTA and Tris was necessary."( Protoplasts from yeast and mycelial forms of Candida albicans.
Riggsby, WS; Torres-Bauzá, LJ, 1980
)
0.58
"Treatment with dithiothreitol reactivated the cystamine- or arginine vasotocin-inactivated enzyme formed in broken cell preparations and the cystamine-inactivated enzyme formed in intact cells."( Evidence of inactivation of pineal indoleamine N-acetyltransferase by protein thiol:disulfide exchange.
Klein, DC; Namboodiri, MA; Weller, JL, 1980
)
0.6
"Treatment with dithiothreitol reduced K(+)-Cl- cotransport activity in SAD-1 and beta-thal/SAD-1 mice to levels similar to that of control strains, indicating that reversible sulfhydryl oxidation contributes to the activated state of K(+)-Cl- cotransport in mouse erythrocytes that express transgenic human Hb SAD."( Sulfhydryl oxidation and activation of red cell K(+)-Cl- cotransport in the transgenic SAD mouse.
Beuzard, Y; Brugnara, C; De Franceschi, L, 1995
)
0.63
"Treatment with dithiothreitol has only a minor effect on the dissociation of the tetramer indicating that the association is not through disulfide formation between the protomers."( Association and dissociation of protein disulfide isomerase.
Tsou, CL; Wang, CC; Yu, XC, 1994
)
0.63
"Treatment with dithiothreitol can thus mimic intracellular activation of the toxin."( Dithiothreitol generates an activated 250,000 mol. wt form of Clostridium difficile toxin B.
Bergman, T; Florin, I; Shoshan, MC; Thelestam, M, 1993
)
2.07
"Pretreatment with dithiothreitol inhibited nociceptin binding to the ORL1 receptor."( Nociceptin activation of the human ORL1 receptor expressed in Chinese hamster ovary cells: functional homology with opioid receptors.
Fawzi, AB; Graziano, MP; Hawes, B; Weig, B; Zhang, H, 1997
)
0.62
"Pretreatment with dithiothreitol (DTT) is necessary to dissolve mucus in samples of induced sputum prior to analysis. "( Flow cytometric analysis of the effect of dithiothreitol on leukocyte surface markers.
Böttcher, M; Gercken, G; Jörres, RA; Loppow, D; Magnussen, H, 2000
)
0.9
"Treatment with dithiothreitol restores much of the transport activity."( Proximity of two oppositely oriented reentrant loops in the glutamate transporter GLT-1 identified by paired cysteine mutagenesis.
Bendahan, A; Brocke, L; Grunewald, M; Kanner, BI, 2002
)
0.65
"Treatment with dithiothreitol before sonication increased the yield of nuclei in suspension and decreased the amount of debris and clumps, thereby suppressing overestimation of small S fractions."( DNA flow cytometry of isolated keratinized epithelia: a methodological study based on ultrasonic tissue disaggregation.
Larsen, JK; Møller, U, 1979
)
0.6
"Treatment with dithiothreitol is a satisfactory method for confirming the content of rubella IgM antibody."( [Detection of rubella specific IgM on gel filtration through Sephadex G 200: use of dithiothreitol and limits with MnCl2-heparine pretreatment (author's transl)].
Daon, F; Freymuth, F; Valdazo, A; Vergnaud, M, 1979
)
0.82
"Treatment with dithiothreitol was necessary for the degradative action of the enzymes to occur."( Changes in the cell surface of the dimorphic forms of Candida albicans by treatment with hydrolytic enzymes.
Barlow, AJ; Chattaway, FW; O'Reilly, J; Shenolikar, S, 1976
)
0.6
"Treatment with dithiothreitol, a reversible reducing reagent, resulted in detection of 3 to 4 isoforms of the glucocorticoid receptor."( The effect of oxidation/reduction on the charge heterogeneity of the human glucocorticoid receptor.
Cidlowski, JA; Silva, CM, 1992
)
0.62
"Treatment with dithiothreitol reduced the number of binding sites by greater than 70%."( Amphibian myocardial angiotensin II receptors are distinct from mammalian AT1 and AT2 receptor subtypes.
Catt, KJ; Ji, H; Millan, MA; Sandberg, K, 1991
)
0.62
"Pretreatment with dithiothreitol (0.2 mM) prevented doxorubicin-induced channel inactivation, and channel activity persisted for an average of 58 minutes."( Biphasic effects of doxorubicin on the calcium release channel from sarcoplasmic reticulum of cardiac muscle.
Borgatta, L; Ehrlich, BE; Kim, DH; Ondrias, K, 1990
)
0.6
"Treatment with dithiothreitol reduced the binding measured with either ligand, and reoxidization of the disulfides fully restored binding."( Sulfhydryl modification of two nicotinic binding sites in mouse brain.
Campbell, SM; Collins, AC; Marks, MJ; Stitzel, JA, 1988
)
0.61
"Treatment with dithiothreitol, neuraminidase, and low pH (3.3) buffer partially dissociated hCG from its receptor with dissociation rates of 42.8%, 35.2%, and 68.7%, respectively."( Dissociation of hCG-receptor complex and detection of hCG receptors in human chorionic tissues.
Chen, F; Furuhashi, Y; Goto, S; Kinoshita, Y; Okamoto, T; Saito, M; Sugiyama, M; Tomoda, Y, 1988
)
0.61
"Treatment of dithiothreitol-reduced thioredoxin with an excess of monobromobimane in Tris buffer (pH 8.0, 23 degrees C) for 30 min resulted in the formation of a stable derivative which was quantitated by reverse-phase high-performance liquid chromatography with fluorescence detection providing sensitivity in the low picomole range."( Determination of thiol proteins using monobromobimane labeling and high-performance liquid chromatographic analysis: application to Escherichia coli thioredoxin.
Chinn, PC; Fahey, RC; Pigiet, V, 1986
)
0.62
"The treatment with dithiothreitol resulted in a decrease in Vmax values but did not alter the Km for Ca2+ for the Na2+-Ca2+ exchange reaction."( Role for sulfur-containing groups in the Na+-Ca2+ exchange of cardiac sarcolemmal vesicles.
Philipson, KD; Pierce, GN; Ward, R, 1986
)
0.59

Toxicity

Catalase or vitamin E showed no protective effect against betaA25-35 Dithiothreitol (DTT), N-acetylcysteine (NAC) and cyclosporine A. inhibition of peroxide detoxifying enzymes enhanced toxicity.

ExcerptReferenceRelevance
"When added to Eagle's Minimum Essential Medium supplemented with 10% bovine serum (MEM-10BS), 1mM cysteine was highly toxic to cultured cells."( Cytotoxicity of cysteine in culture media.
Nakayasu, M; Nishiuch, Y; Oikawa, A; Sasaki, M, 1976
)
0.26
" In contrast, oxidized DTT did not enhance NMDA toxicity nor was it toxic when added alone."( The action of CGS-19755 on the redox enhancement of NMDA toxicity in rat cortical neurons in vitro.
Aizenman, E; Hartnett, KA, 1992
)
0.28
" This suggests that DEDC acts as a trap for the toxic quinoneimines, thus preventing alkylation of essential macromolecules."( Molecular mechanism for prevention of N-acetyl-p-benzoquinoneimine cytotoxicity by the permeable thiol drugs diethyldithiocarbamate and dithiothreitol.
Lauriault, VV; O'Brien, PJ, 1991
)
0.48
" SDS-PAGE of the toxic fraction showed a single band with a Mr of about 150,000, and after dithiothreitol treatment, two bands with Mr of 100,000 and 50,000."( Detection of neutral sugars in purified type G botulinum progenitor toxin and the effects of some glycolytic enzymes on its molecular dissociation and oral toxicity.
Miyata, T; Nukina, M; Sakaguchi, G; Sakaguchi, S, 1991
)
0.5
" DPPD was able to block the toxicity of two other toxic cysteine conjugates S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine and S-(1,1,2,2-tetrafluoroethyl)-L-cysteine."( The mechanism of cysteine conjugate cytotoxicity in renal epithelial cells. Covalent binding leads to thiol depletion and lipid peroxidation.
Brown, PC; Chen, Q; Jones, TW; Stevens, JL, 1990
)
0.28
"The disulfide metabolites of thiono-sulfur drugs were found to be about 50 to 100 times more toxic to isolated rat hepatocytes than the corresponding parent drugs."( The toxicity of disulphides to isolated hepatocytes and mitochondria.
Jatoe, SD; Lauriault, V; McGirr, LG; O'Brien, PJ, 1988
)
0.27
"N-acetyl-p-benzoquinone imine (NAPQI), a reactive metabolite of acetaminophen, has previously been shown to be toxic to hepatocytes freshly isolated from rat liver [Mol."( Comparative cytotoxic effects of N-acetyl-p-benzoquinone imine and two dimethylated analogues.
Cotgreave, IA; Harvison, PJ; Moldéus, P; Nelson, SD; Porubek, DJ; Rundgren, M, 1988
)
0.27
" As well as its effect in reducing the formation of the reactive metabolite, DTT has a potent protective effect against the toxic processes initiated by the APAP reactive metabolite."( Comparison of the protective effects of N-acetylcysteine, 2-mercaptopropionylglycine and dithiothreitol against acetaminophen toxicity in mouse hepatocytes.
Harman, AW; Self, G, 1986
)
0.49
" Species differences in sensitivity to paracetamol toxicity were shown to be due to differences in the rate of oxidation of the drug to its toxic metabolite."( Freshly isolated hepatocytes as a model for studying the toxicity of paracetamol.
Boobis, AR; Davies, DS; Hampden, CE; Tee, LB,
)
0.13
" Of the scavengers of toxic oxygen metabolites tested only the hydroxyl radical scavenger sodium benzoate inhibited cytotoxicity."( Importance of oxidative metabolism in T cell cytotoxicity: a comparison of cloned T cells and spleen cells.
Franks, D; Thorne, KJ, 1983
)
0.27
"5 mM DTT is safe and provides mucus-free monolayers for immunocytochemistry and single-cell suspensions for flow cytometry."( Safe separation of sputum cells from mucoid glycoprotein.
Cavenaugh, LL; Erozan, YS; Li, L; Qiao, Y; Sharma, R; Tockman, MS; Zhao, GZ,
)
0.13
"We examined the effect of a toxic concentration of allyl alcohol (0."( Allyl alcohol cytotoxicity in isolated rat hepatocytes: mechanism of cell death does not involve an early rise in cytosolic free calcium.
Cai, Y; Hornbrook, KR; Rikans, LE, 1994
)
0.29
" In comparisons of the toxic effects of PG and its metabolites at concentrations of 2 mM, the parent compound PG was the most toxic."( Metabolism and cytotoxicity of propyl gallate in isolated rat hepatocytes: effects of a thiol reductant and an esterase inhibitor.
Moldéus, P; Nakagawa, Y; Nakajima, K; Tayama, S, 1995
)
0.29
"5-2 mmol l-1) ameliorated all these toxic effects of cisplatin in a concentration related manner."( Amelioration of cisplatin toxicity in rat renal cortical slices by dithiothreitol in vitro.
Lindup, WE; Ma, XL; Xia, YX; Zhang, JG; Zhang, M; Zhong, LF, 1994
)
0.52
"0 mM thiol, but is not seen at higher or lower drug concentrations; N-acetylcysteine (NAC) is toxic only at concentrations > or = 2 mM and shows no biphasic pattern; and glutathione (GSH) and penicillamine are only minimally toxic at all concentrations."( Mechanisms for the oxygen radical-mediated toxicity of various thiol-containing compounds in cultured mammalian cells.
Biaglow, JE; Held, KD, 1994
)
0.29
" The results suggest that initial events in the toxic process are reversible, and that DTT can prevent cytotoxicity if added to hepatocytes before irreversible damage occurs; however, the mechanism by which DTT exerts its protection is not clear."( Dithiothreitol reversal of allyl alcohol cytotoxicity in isolated rat hepatocytes.
Cai, Y; Rikans, LE, 1994
)
1.73
"OH, the ultimate toxic species, via the metal-catalyzed Fenton reaction."( Role of the pentose cycle in oxygen radical-mediated toxicity of the thiol-containing radioprotector dithiothreitol in mammalian cells.
Biaglow, JE; Held, KD; Tuttle, SW, 1993
)
0.5
"We have previously reported that incubation of isolated rat hepatocytes with the antimicrobial drug nitrofurantoin causes toxic oxidative stress as a result of oxygen activation by futile one-electron redox cycling."( Molecular mechanisms of nitrofurantoin-induced hepatocyte toxicity in aerobic versus hypoxic conditions.
Khan, S; O'Brien, PJ; Silva, JM, 1993
)
0.29
"Under certain conditions, many radioprotective thiols can be toxic, causing loss of colony-forming ability in cultured mammalian cells in a biphasic fashion whereby the thiols are not toxic at high or low concentrations of the drug, but cause decreased clonogenicity at intermediate (0."( Role of Fenton chemistry in thiol-induced toxicity and apoptosis.
Biaglow, JE; Held, KD; Hopcia, KL; Sylvester, FC, 1996
)
0.29
" Pretreatment of hepatocytes with medium deficient in sulfur amino acids accelerated cell death induced by EMS, confirming the previously reported cytoprotective role for GSH in this toxic event."( Role of cellular thiol status in tocopheryl hemisuccinate cytoprotection against ethyl methanesulfonate-induced toxicity.
Bryson, KF; Fariss, MW; Tirmenstein, MA, 1997
)
0.3
" Previous work has shown that 3,4-dichloroaniline is acutely toxic to the kidney and bladder."( 3,4-Dichlorophenylhydroxylamine cytotoxicity in renal cortical slices from Fischer 344 rats.
Ball, JG; Rankin, GO; Stoll, S; Valentovic, M, 2001
)
0.31
" Catalase or vitamin E showed no protective effect against betaA25-35 Dithiothreitol (DTT), N-acetylcysteine (NAC) and cyclosporine A significantly prevented the toxic effects of both betaA25-35 and peroxide, while inhibition of peroxide detoxifying enzymes enhanced toxicity."( beta-Amyloid-induced cytotoxicity, peroxide generation and blockade of glutamate uptake in cultured astrocytes.
Brera, B; de Ceballos, ML; Fernández-Tomé, MP, 2001
)
0.54
" These findings indicate that 2A45CP is directly toxic to renal cortical slices and that cytotoxicity is at least partially mediated by a reactive intermediate."( Characterization of 2-amino-4,5-dichlorophenol (2A45CP) in vitro toxicity in renal cortical slices from male Fischer 344 rats.
Ball, JG; Rankin, GO; Sun, H; Valentovic, MA, 2002
)
0.31
"Arsenic, a common environmental pollutant, is toxic to many mammalian cells."( Comparison of the cytotoxicity induced by different exposure to sodium arsenite in two fish cell lines.
Chaung, RH; Tung, LC; Wang, YC, 2004
)
0.32
"Primaquine-induced hemolytic anemia is a toxic side effect that is due to premature splenic sequestration of intact erythrocytes."( Primaquine-induced hemolytic anemia: role of membrane lipid peroxidation and cytoskeletal protein alterations in the hemotoxicity of 5-hydroxyprimaquine.
Bowman, ZS; Jollow, DJ; McMillan, DC; Morrow, JD, 2005
)
0.33
"It is well-known that organotellurium compounds can have antioxidant activity in vitro, but in vivo these compounds can be potentially toxic to rodents."( Diethyl 2-phenyl-2 tellurophenyl vinylphosphonate: an organotellurium compound with low toxicity.
Beque, MC; Braga, AL; de Avila, DS; Folmer, V; Nogueira, CW; Rocha, JB; Soares, FA; Zeni, G, 2006
)
0.33
" A molybdenum-dependent mitochondrial enzyme, sulfite oxidase, oxidizes sulfite to inorganic sulfate and prevents its toxic effects."( Mechanism of sulfite cytotoxicity in isolated rat hepatocytes.
Niknahad, H; O'Brien, PJ, 2008
)
0.35
" These findings suggest that the toxic effect of thiol oxidants present during chronic gastritis is partially due to dysregulation of [Zn(2+)](i) early in the process and that zinc chelation can protect, but not rescue, gastric glands exposed to toxic doses of NH(2)Cl."( Monochloramine-induced toxicity and dysregulation of intracellular Zn2+ in parietal cells of rabbit gastric glands.
Blass, AL; Dubach, JM; Kohler, JE; Naik, HB; Soybel, DI; Tai, K, 2010
)
0.36
" These results suggest that the toxic effect of MCT on hepatocytes may be caused by metabolite-induced mitochondrial energetic impairment, together with a decrease of cellular glutathione and protein thiols."( Cytotoxicity of monocrotaline in isolated rat hepatocytes: effects of dithiothreitol and fructose.
Alves, LC; Garcia, AF; Maioli, MA; Mingatto, FE; Perandin, D; Pereira, FT, 2011
)
0.6
"The link between emissions of vehicular particulate matter (PM) and adverse health effects is well established."( Cell toxicity and oxidative potential of engine exhaust particles: impact of using particulate filter or biodiesel fuel blend.
Cassee, FR; Gerlofs-Nijland, ME; Låg, M; Leseman, DL; Ntziachristos, L; Samaras, Z; Schwarze, P; Totlandsdal, AI; Tzamkiozis, T, 2013
)
0.39
" Cellular ALR exerts its lipid lowering and anti-apoptotic actions by enhancing FABP1, which binds toxic FFA, increasing mitochondrial β-oxidation by elevating the mitochondrial FFA transporter CPT1α, and decreasing ELOVL6, which delivers toxic FFA metabolites."( Attenuated lipotoxicity and apoptosis is linked to exogenous and endogenous augmenter of liver regeneration by different pathways.
Buechler, C; Dayoub, R; Hofmann, U; Ibrahim, S; Lorenz, J; Lupke, M; Melter, M; Ruemmele, P; Weiss, TS, 2017
)
0.46

Pharmacokinetics

ExcerptReferenceRelevance
" The holoenzyme of DTT-treated PEG-METase gave a several times larger area under the plasma concentration curve than that of DTT-untreated PEG-METase, not because of an increase of the half-life but because of high specific activity."( Physicochemical and pharmacokinetic characterization of highly potent recombinant L-methionine gamma-lyase conjugated with polyethylene glycol as an antitumor agent.
Esaki, N; Hoffman, RM; Inagaki, K; Ito, T; Kobayashi, Y; Nagatome, H; Notsu, Y; Ohno, M; Takakura, T; Takimoto, A; Yagi, S; Yoshida, H; Yoshioka, T, 2006
)
0.33

Compound-Compound Interactions

ExcerptReferenceRelevance
" Before injection of the spermatozoa, we quantified the effects of sperm capacitation combined with sperm pretreatment on the acrosome and plasma membrane status."( Sperm capacitation combined with removal of the sperm acrosome and plasma membrane enhances paternal nucleus remodelling and early development of bovine androgenetic embryos.
Ahmad, S; Bai, L; Huo, L; Li, W; Li, X; Wang, X; Xiao, Y; Yang, L; Zhang, H; Zhang, X, 2013
)
0.39
"The extensively used thiol antioxidants (dithiothreitol, glutathione, and N-acetylcysteine) in combination with hydroxycobalamine (vitamin B12) gain toxic activity in relation to human lymphocytic leukemia cell line HL60."( Thiol antioxidants in combination with vitamin B12 induce apoptotic death of human lymphocytic leukemia cells by destabilization of lysosomes with the involvement of iron ions.
Akatov, VS; Faskhutdinova, AA; Solovyev, VV; Solovyeva, ME, 2013
)
0.66

Bioavailability

ExcerptReferenceRelevance
" This study provides the first evidence that increased denitrosylation leads to increased bioavailability of NO, independent of NOS activity, to promote sustained angiogenesis."( The release of nitric oxide from S-nitrosothiols promotes angiogenesis.
Ahmad, S; Ahmed, A; Ahmed, S; Al-Ani, B; Cudmore, M; Fujisawa, T; Hewett, PW, 2006
)
0.33
" The present study demonstrated that iNOS-derived superoxide generation was reduced, and that the NO bioavailability was increased, by treatment with the NOS-cofactor, tetrahydrobiopterin (BH4), before I/R in the hearts isolated from diabetic rats."( Reversal of inducible nitric oxide synthase uncoupling unmasks tolerance to ischemia/reperfusion injury in the diabetic rat heart.
Fujita, M; Ito, S; Iwasaka, T; Katano, T; Okazaki, T; Otani, H; Shimazu, T; Yoshioka, K, 2011
)
0.37

Dosage Studied

Dithiothreitol has two major effects on receptor function. It shifts the dose-response curve for agonist-induced increases in 22Na+ permeability to 10-fold higher concentrations. It decreases the binding affinity of the receptor for the same agonist about 6-fold.

ExcerptRelevanceReference
" Sigmoidal dose-response curves were obtained, similar to those obtained previously for stimulation by the same agonists of the hydrolysis of phosphatidylcholine by phospholipase A2 (Gullis & Rowe, 1975a)."( The stimulation by synaptic transmitters of the incorporation of oleate into the phospholipid of synaptic membranes.
Gullis, RJ; Rowe, CE, 1975
)
0.25
" As a result of enzyme purification, there is an alteration of the dose-response relationship for nitric oxide activation."( Effects of thiols, sugars, and proteins on nitric oxide activation of guanylate cyclase.
Braughler, JM; Mittal, CK; Murad, F, 1979
)
0.26
" In addition, our preparation did not demonstrate the long-lasting responses to bromoaTT-induced depression of the nicotinic responses was studied on the dose-response curves; the mode of receptor inhibition was rather complexed, being neither type of competitive nor non-competitive."( Effects of disulfide bond reduction on the excitatory and inhibitory postsynaptic responses of Aplysia ganglion cells.
Sato, M; Sato, T; Sawada, M, 1976
)
0.26
" Similarly, injection of PTU in rats in a dosage of 5 microgram/100 g BW or greater significantly impaired T4 5'-deiodination in subsequently isolated kidney microsomal preparations."( Thyroxine 5'-deiodinase activity of rat kidney: observations on activation by thiols and inhibition by propylthiouracil.
Leonard, JL; Rosenberg, IN, 1978
)
0.26
" The dose-response curve for iontophoretically applied ACh indicates that neither the total number of ionic channels nor the cooperativity within the receptors are changed."( Acetylcholine receptor: modification of synaptic gating mechanism after treatment with a disulfide bond reducing agent.
Ben-Haim, D; Dreyer, F; Peper, K, 1975
)
0.25
" The dose-response relationships are identical for labeled and native hormone in all three systems."( Further studies on acetamidination as a technique for preparation of a biologically valid 3-H-labeled tracer for parathyroid hormone.
Chuang, J; Zull, JE, 1975
)
0.25
"N-ethylmaleimide which is known to react irreversibly with free -SH groups of protein when incubated with rabbit aorta (alpha-adrenoreceptor) or atria (beta-adrenoreceptor) markedly depressed the dose-response curves of norepinephrine isomers in the aorta but not in atria."( Influence of group selective reagents in tissues containing alpha- and beta-adrenoceptors.
Chai, HS; Miller, DD; Patil, PN; Salman, KN, 1976
)
0.26
" NADPH shifts the dose-response curve of NO to the left and possibly increases, in this way, the ADP-ribosylation reaction under physiological conditions."( NADPH: a stimulatory cofactor for nitric oxide-induced ADP-ribosylation reaction.
Brüne, B; Dimmeler, S; Lapetina, EG, 1992
)
0.28
" DTT treatment also markedly shifted the dose-response curve of NMDA to the left."( Redox modulation of N-methyl-D-aspartate-stimulated neurotransmitter release from rat brain slices.
Blair, R; Woodward, JJ, 1991
)
0.28
" The dose-response relationship was inferred from Hill (double-log) plots for myoballs bathed in 500 nM-cis-Bis-Q at three membrane potentials."( Dose-response of acetylcholine receptor channels opened by a flash-activated agonist in voltage-clamped rat myoballs.
Chabala, LD; Gurney, AM; Lester, HA, 1986
)
0.27
"Solutions of synthetic fecapentaene 12 (FP-12) intended for carcinogenicity studies were found to decompose extremely rapidly during customary dosage procedures."( Decomposition and quality control considerations in biological work with fecapentaene preparations.
Andrews, AW; Anjo, T; Bradford, WW; Donovan, PJ; Keefer, LK; Ohannesian, L; Reist, EJ; Sheffels, PR; Streeter, AJ; Wu, PP,
)
0.13
" This correlated with the dose-response required to stimulate phosphorylase activity in intact hepatocytes and suggests that the effects of the opioid peptides on carbohydrate metabolism in liver are the result of cross-reactivity of the peptides with angiotensin II receptors."( [Leu]enkephalin stimulates carbohydrate metabolism in isolated hepatocytes and kidney tubule fragments by interaction with angiotensin II receptors.
Hothi, SK; Randall, DP; Titheradge, MA, 1989
)
0.28
" Conversely, following potentiation of the response to histamine with DTT, exposure of the tissue to desensitizing concentrations of histamine resulted in a dextral shift of the dose-response curve (dose ratio = 39."( Selective enhancement of histamine H1-receptor responses in guinea-pig ileal smooth muscle by 1,4-dithiothreitol.
Donaldson, J; Hill, SJ, 1986
)
0.49
" A comparison of the inhibitory effects of 2-acetylpyridine thiosemicarbazone itself on viral reductase and on virus replication in vitro demonstrated a similarity in the dose-response relationships for the two parameters."( Selective inhibition of herpes simplex virus ribonucleoside diphosphate reductase by derivatives of 2-acetylpyridine thiosemicarbazone.
Drach, JC; Shipman, C; Turk, SR, 1986
)
0.27
" While the dose-response curves for [3H]dexamethasone binding versus thiol reagent are normally sigmoidal, an unusual bimodal curve is obtained with MMTS in which dexamethasone binding is eliminated at low, but maintained at intermediate, MMTS concentrations."( Steroid binding to hepatoma tissue culture cell glucocorticoid receptors involves at least two sulfhydryl groups.
Miller, NR; Simons, SS, 1988
)
0.27
" Dose-response studies of GS-Mal treatment of intact cells suggested that some functional carriers lack a reactive external sulfhydryl, which can be partially regenerated by pretreatment with excess cysteine."( Reaction of an exofacial sulfhydryl group on the erythrocyte hexose carrier with an impermeant maleimide. Relevance to the mechanism of hexose transport.
May, JM, 1988
)
0.27
"45 mmol/l) the otherwise bell-shaped dose-response curve for conditioned medium changed to a sigmoid curve."( Vitamin C and thiol reagents promote the in vitro growth of murine granulocyte/macrophage progenitor cells by neutralizing endogenous inhibitor(s).
Helgestad, J; Lie, SO; Storm-Mathisen, I, 1986
)
0.27
" After dosing with triethyl lead, in vivo inhibition of ALAD only occurred at the high dose, but activation analysis in vitro showed increased ALAD activity to be present at all dose levels in a dose-dependent fashion."( Kinetic parameters of the inhibition of red blood cell aminolevulinic acid dehydratase by triethyl lead and its reversal by dithiothreitol and zinc.
Villeneuve, DC; Yagminas, AP, 1987
)
0.48
" Treatment of strips with PCMB and DTNB did not alter the dose-response curves for GTN."( Investigations into the role of sulfhydryl groups in the mechanism of action of the nitrates.
Armstrong, PW; Marks, GS; Moffat, JA, 1982
)
0.26
"The addition of 1 X 10(-3) M or 1 X 10(-2) M 2-mercaptoethanol (2-MEt), a sulfhydryl reagent, produced a leftward displacement (potentiation) of the dose-response curves of mesenteric arterial strips for histamine, norepinephrine, serotonin, angiotensin II, prostaglandin F2 alpha and KCl."( Alterations in pharmacological receptor activities of rabbit arteries by sulfhydryl reagents.
Asano, M; Hidaka, H, 1983
)
0.27
" To explain sigmoidal dose-response curves, a two-site model is already sufficient."( Interaction of cholinergic ligands with the purified acetylcholine receptor protein. I. Equilibrium binding studies.
Maelicke, A; Prinz, H, 1983
)
0.27
"Chemical modification of membrane-bound Torpedo californica acetylcholine receptor by the disulfide reducing agent dithiothreitol has two major effects on receptor function: (1) it shifts the dose-response curve for agonist-induced increases in 22Na+ permeability to 10-fold higher concentrations, and (2) it decreases the binding affinity of the receptor for the same agonist about 6-fold."( Effects of thio-group modifications on the ion permeability control and ligand binding properties of Torpedo californica acetylcholine receptor.
Lukas, RJ; McNamee, MG; Walker, JW, 1981
)
0.47
" Dose-response measurements show that exposure of alpha H186C mutants to MMTS causes a shift in apparent agonist affinity without changing the peak response, and this is not reversible by DTT."( Covalent modification of engineered cysteines in the nicotinic acetylcholine receptor agonist-binding domain inhibits receptor activation.
Hawrot, E; McLaughlin, JT; Yellen, G, 1995
)
0.29
" When infected cells were treated with DTT, the NTPase was activated in a dose-response fashion, as assessed by migration on SDS-polyacrylamide gel electrophoresis and by an increase in enzymatic activity."( Induced activation of the Toxoplasma gondii nucleoside triphosphate hydrolase leads to depletion of host cell ATP levels and rapid exit of intracellular parasites from infected cells.
Beckers, C; Joiner, KA; Nakaar, V; Qi, H; Riehl, A; Silverman, JA, 1998
)
0.3
" The dose-response increase of coproporphyrin secretion accompanied by the depression of CO activity supports the suggestion that lead causes CO inhibition, as observed in this cellular model."( Effect of acute lead treatment on coproporphyrinogen oxidase activity in HepG2 cells.
Garciá Vargas, G; Gutiérrez-Ruiz, MC; Hernández, E, 1998
)
0.3
" The antisecretory action of YJA20379-1 was short lasting (less than 7 h at an oral dosing of 30 mg/kg)."( Biochemical and pharmacological characteristics of a newly synthesized H+-K+ ATPase inhibitor, YJA20379-1, 2-amino-4,5-dihydro-8-phenylimidazole[2,1-b]thiazolo[5,4-g]benzothiazol e.
Chang, MS; Choi, WS; Chung, YK; Kim, KB; Lee, SB; Sohn, SK; Woo, TW, 1999
)
0.3
" The noncompetitive antagonist MK-801 and a glycine-site blocker were equally neuroprotective in both normal and reduced conditions, but there was a significant rightward shift in the dose-response curves of the competitive antagonists APV and CPP and the uncompetitive antagonist memantine."( Reducing conditions significantly attenuate the neuroprotective efficacy of competitive, but not other NMDA receptor antagonists in vitro.
Eshak, M; Iannotti, F; Pringle, AK; Self, J, 2000
)
0.31
" Dose-response data are consistent with a scheme in which two SNDTT molecules bind sequentially to a single channel, with binding of the first being sufficient to produce block."( Selective open-channel block of Shaker (Kv1) potassium channels by s-nitrosodithiothreitol (SNDTT).
Brock, MW; Gilly, WF; Mathes, C, 2001
)
0.54
" A Zn(2+) chelating agent, tricine, potentiated GABA currents for the alphabeta constructs and vertically displaced GABA dose-response curves, suggesting that these receptors are subject to some inhibition by basal Zn(2+)."( Redox modulation of GABAA receptors obscured by Zn2+ complexation.
Smart, TG; Wilkins, ME, 2002
)
0.31
" Hits were tested in dose-response both in the dithiothreitol (DTT)-containing buffer used in the primary HTS and in buffer containing cysteine in place of DTT to rule out artifacts due to oxidative inactivation of the enzyme."( Evaluation of an orthogonal pooling strategy for rapid high-throughput screening of proteases.
Diamond, SL; Motlekar, N; Napper, AD, 2008
)
0.6
" Weak genotoxic activity was detected for [CuL](+) and [CuL'](+), with a significative dose-response effect for [CuL'](+), which was shown to be more cytotoxic in the Ames test and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assays."( Biological assays and noncovalent interactions of pyridine-2-carbaldehyde thiosemicarbazonecopper(II) drugs with [poly(dA-dT)](2), [poly(dG-dC)] (2), and calf thymus DNA.
Borrás, J; Busto, N; García, B; Garcia-Tojal, J; Gaspar, J; Gil-García, R; González-Alvarez, M; Ibeas, S; Leal, JM; Martins, C; Ruiz, R, 2010
)
0.36
" These peptides, which compete with LEDGF for binding to IN, displayed an intriguing equilibrium binding dose-response curve characterized by a plateau rising to a peak, then descending to a second plateau."( Dithiothreitol causes HIV-1 integrase dimer dissociation while agents interacting with the integrase dimer interface promote dimer formation.
Brendza, KM; Geleziunas, R; Hung, M; Jin, D; Jones, GS; Liu, X; Mitchell, M; Mukund, S; Niedziela-Majka, A; Novikov, N; Sakowicz, R; Samuel, D; Tsiang, M, 2011
)
1.81
" Lower intact FVIII amounts in Emoclot might be mainly due to the low von Willebrand factor dosage and the absence of albumin."( Plasma-derived clotting factor VIII: heterogeneity evaluation in the quest for potential inhibitory-antibody stimulating factors.
Blasi, B; D'Alessandro, A; D'Amici, GM; Vaglio, S; Zolla, L, 2011
)
0.37
"Warfarin dose-response curves fit to the secreted FIX activity data for coexpressed hVKORC1 wild-type, Val29Leu, Val45Ala and Leu128Arg variants."( A new cell culture-based assay quantifies vitamin K 2,3-epoxide reductase complex subunit 1 function and reveals warfarin resistance phenotypes not shown by the dithiothreitol-driven VKOR assay.
Bevans, CG; Czogalla, KJ; Fregin, A; Gansler, J; Müller, CR; Oldenburg, J; Rost, S; Taverna, M; Watzka, M, 2013
)
0.59
" However, various studies based on this assay have reported warfarin dose-response data, usually summarized as half-maximal inhibitory concentration (IC50), that vary over orders of magnitude and reflect the broad range of conditions used to obtain VKOR assay data."( Determination of the warfarin inhibition constant Ki for vitamin K 2,3-epoxide reductase complex subunit-1 (VKORC1) using an in vitro DTT-driven assay.
Bevans, CG; Koßmann, K; Krettler, C; Oldenburg, J; Reinhart, C; Tran, H; Watzka, M, 2013
)
0.39
"Single nucleotide polymorphisms in the vitamin K epoxide reductase (VKOR) gene have been successfully used for warfarin dosage prediction."( Evaluation of warfarin resistance using transcription activator-like effector nucleases-mediated vitamin K epoxide reductase knockout HEK293 cells.
Jin, DY; Stafford, DW; Tie, JK; Tie, K, 2013
)
0.39
"Findings will provide timely information on the safety, efficacy, and optimal dosing of t-PA to treat moderate/severe COVID-19-induced ARDS, which can be rapidly adapted to a phase III trial (NCT04357730; FDA IND 149634)."(
Abbasi, S; Abd El-Wahab, A; Abdallah, M; Abebe, G; Aca-Aca, G; Adama, S; Adefegha, SA; Adidigue-Ndiome, R; Adiseshaiah, P; Adrario, E; Aghajanian, C; Agnese, W; Ahmad, A; Ahmad, I; Ahmed, MFE; Akcay, OF; Akinmoladun, AC; Akutagawa, T; Alakavuklar, MA; Álava-Rabasa, S; Albaladejo-Florín, MJ; Alexandra, AJE; Alfawares, R; Alferiev, IS; Alghamdi, HS; Ali, I; Allard, B; Allen, JD; Almada, E; Alobaid, A; Alonso, GL; Alqahtani, YS; Alqarawi, W; Alsaleh, H; Alyami, BA; Amaral, BPD; Amaro, JT; Amin, SAW; Amodio, E; Amoo, ZA; Andia Biraro, I; Angiolella, L; Anheyer, D; Anlay, DZ; Annex, BH; Antonio-Aguirre, B; Apple, S; Arbuznikov, AV; Arinsoy, T; Armstrong, DK; Ash, S; Aslam, M; Asrie, F; Astur, DC; Atzrodt, J; Au, DW; Aucoin, M; Auerbach, EJ; Azarian, S; Ba, D; Bai, Z; Baisch, PRM; Balkissou, AD; Baltzopoulos, V; Banaszewski, M; Banerjee, S; Bao, Y; Baradwan, A; Barandika, JF; Barger, PM; Barion, MRL; Barrett, CD; Basudan, AM; Baur, LE; Baz-Rodríguez, SA; Beamer, P; Beaulant, A; Becker, DF; Beckers, C; Bedel, J; Bedlack, R; Bermúdez de Castro, JM; Berry, JD; Berthier, C; Bhattacharya, D; Biadgo, B; Bianco, G; Bianco, M; Bibi, S; Bigliardi, AP; Billheimer, D; Birnie, DH; Biswas, K; Blair, HC; Bognetti, P; Bolan, PJ; Bolla, JR; Bolze, A; Bonnaillie, P; Borlimi, R; Bórquez, J; Bottari, NB; Boulleys-Nana, JR; Brighetti, G; Brodeur, GM; Budnyak, T; Budnyk, S; Bukirwa, VD; Bulman, DM; Burm, R; Busman-Sahay, K; Butcher, TW; Cai, C; Cai, H; Cai, L; Cairati, M; Calvano, CD; Camacho-Ordóñez, A; Camela, E; Cameron, T; Campbell, BS; Cansian, RL; Cao, Y; Caporale, AS; Carciofi, AC; Cardozo, V; Carè, J; Carlos, AF; Carozza, R; Carroll, CJW; Carsetti, A; Carubelli, V; Casarotta, E; Casas, M; Caselli, G; Castillo-Lora, J; Cataldi, TRI; Cavalcante, ELB; Cavaleiro, A; Cayci, Z; Cebrián-Tarancón, C; Cedrone, E; Cella, D; Cereda, C; Ceretti, A; Ceroni, M; Cha, YH; Chai, X; Chang, EF; Chang, TS; Chanteux, H; Chao, M; Chaplin, BP; Chaturvedi, S; Chaturvedi, V; Chaudhary, DK; Chen, A; Chen, C; Chen, HY; Chen, J; Chen, JJ; Chen, K; Chen, L; Chen, Q; Chen, R; Chen, SY; Chen, TY; Chen, WM; Chen, X; Chen, Y; Cheng, G; Cheng, GJ; Cheng, J; Cheng, YH; Cheon, HG; Chew, KW; Chhoker, S; Chiu, WN; Choi, ES; Choi, MJ; Choi, SD; Chokshi, S; Chorny, M; Chu, KI; Chu, WJ; Church, AL; Cirrincione, A; Clamp, AR; Cleff, MB; Cohen, M; Coleman, RL; Collins, SL; Colombo, N; Conduit, N; Cong, WL; Connelly, MA; Connor, J; Cooley, K; Correa Ramos Leal, I; Cose, S; Costantino, C; Cottrell, M; Cui, L; Cundall, J; Cutaia, C; Cutler, CW; Cuypers, ML; da Silva Júnior, FMR; Dahal, RH; Damiani, E; Damtie, D; Dan-Li, W; Dang, Z; Dasa, SSK; Davin, A; Davis, DR; de Andrade, CM; de Jong, PL; de Oliveira, D; de Paula Dorigam, JC; Dean, A; Deepa, M; Delatour, C; Dell'Aiera, S; Delley, MF; den Boer, RB; Deng, L; Deng, Q; Depner, RM; Derdau, V; Derici, U; DeSantis, AJ; Desmarini, D; Diffo-Sonkoue, L; Divizia, M; Djenabou, A; Djordjevic, JT; Dobrovolskaia, MA; Domizi, R; Donati, A; Dong, Y; Dos Santos, M; Dos Santos, MP; Douglas, RG; Duarte, PF; Dullaart, RPF; Duscha, BD; Edwards, LA; Edwards, TE; Eichenwald, EC; El-Baba, TJ; Elashiry, M; Elashiry, MM; Elashry, SH; Elliott, A; Elsayed, R; Emerson, MS; Emmanuel, YO; Emory, TH; Endale-Mangamba, LM; Enten, GA; Estefanía-Fernández, K; Estes, JD; Estrada-Mena, FJ; Evans, S; Ezra, L; Faria de, RO; Farraj, AK; Favre, C; Feng, B; Feng, J; Feng, L; Feng, W; Feng, X; Feng, Z; Fernandes, CLF; Fernández-Cuadros, ME; Fernie, AR; Ferrari, D; Florindo, PR; Fong, PC; Fontes, EPB; Fontinha, D; Fornari, VJ; Fox, NP; Fu, Q; Fujitaka, Y; Fukuhara, K; Fumeaux, T; Fuqua, C; Fustinoni, S; Gabbanelli, V; Gaikwad, S; Gall, ET; Galli, A; Gancedo, MA; Gandhi, MM; Gao, D; Gao, K; Gao, M; Gao, Q; Gao, X; Gao, Y; Gaponenko, V; Garber, A; Garcia, EM; García-Campos, C; García-Donas, J; García-Pérez, AL; Gasparri, F; Ge, C; Ge, D; Ge, JB; Ge, X; George, I; George, LA; Germani, G; Ghassemi Tabrizi, S; Gibon, Y; Gillent, E; Gillies, RS; Gilmour, MI; Goble, S; Goh, JC; Goiri, F; Goldfinger, LE; Golian, M; Gómez, MA; Gonçalves, J; Góngora-García, OR; Gonul, I; González, MA; Govers, TM; Grant, PC; Gray, EH; Gray, JE; Green, MS; Greenwald, I; Gregory, MJ; Gretzke, D; Griffin-Nolan, RJ; Griffith, DC; Gruppen, EG; Guaita, A; Guan, P; Guan, X; Guerci, P; Guerrero, DT; Guo, M; Guo, P; Guo, R; Guo, X; Gupta, J; Guz, G; Hajizadeh, N; Hamada, H; Haman-Wabi, AB; Han, TT; Hannan, N; Hao, S; Harjola, VP; Harmon, M; Hartmann, MSM; Hartwig, JF; Hasani, M; Hawthorne, WJ; Haykal-Coates, N; Hazari, MS; He, DL; He, P; He, SG; Héau, C; Hebbar Kannur, K; Helvaci, O; Heuberger, DM; Hidalgo, F; Hilty, MP; Hirata, K; Hirsch, A; Hoffman, AM; Hoffmann, JF; Holloway, RW; Holmes, RK; Hong, S; Hongisto, M; Hopf, NB; Hörlein, R; Hoshino, N; Hou, Y; Hoven, NF; Hsieh, YY; Hsu, CT; Hu, CW; Hu, JH; Hu, MY; Hu, Y; Hu, Z; Huang, C; Huang, D; Huang, DQ; Huang, L; Huang, Q; Huang, R; Huang, S; Huang, SC; Huang, W; Huang, Y; Huffman, KM; Hung, CH; Hung, CT; Huurman, R; Hwang, SM; Hyun, S; Ibrahim, AM; Iddi-Faical, A; Immordino, P; Isla, MI; Jacquemond, V; Jacques, T; Jankowska, E; Jansen, JA; Jäntti, T; Jaque-Fernandez, F; Jarvis, GA; Jatt, LP; Jeon, JW; Jeong, SH; Jhunjhunwala, R; Ji, F; Jia, X; Jia, Y; Jian-Bo, Z; Jiang, GD; Jiang, L; Jiang, W; Jiang, WD; Jiang, Z; Jiménez-Hoyos, CA; Jin, S; Jobling, MG; John, CM; John, T; Johnson, CB; Jones, KI; Jones, WS; Joseph, OO; Ju, C; Judeinstein, P; Junges, A; Junnarkar, M; Jurkko, R; Kaleka, CC; Kamath, AV; Kang, X; Kantsadi, AL; Kapoor, M; Karim, Z; Kashuba, ADM; Kassa, E; Kasztura, M; Kataja, A; Katoh, T; Kaufman, JS; Kaupp, M; Kehinde, O; Kehrenberg, C; Kemper, N; Kerr, CW; Khan, AU; Khan, MF; Khan, ZUH; Khojasteh, SC; Kilburn, S; Kim, CG; Kim, DU; Kim, DY; Kim, HJ; Kim, J; Kim, OH; Kim, YH; King, C; Klein, A; Klingler, L; Knapp, AK; Ko, TK; Kodavanti, UP; Kolla, V; Kong, L; Kong, RY; Kong, X; Kore, S; Kortz, U; Korucu, B; Kovacs, A; Krahnert, I; Kraus, WE; Kuang, SY; Kuehn-Hajder, JE; Kurz, M; Kuśtrowski, P; Kwak, YD; Kyttaris, VC; Laga, SM; Laguerre, A; Laloo, A; Langaro, MC; Langham, MC; Lao, X; Larocca, MC; Lassus, J; Lattimer, TA; Lazar, S; Le, MH; Leal, DB; Leal, M; Leary, A; Ledermann, JA; Lee, JF; Lee, MV; Lee, NH; Leeds, CM; Leeds, JS; Lefrandt, JD; Leicht, AS; Leonard, M; Lev, S; Levy, K; Li, B; Li, C; Li, CM; Li, DH; Li, H; Li, J; Li, L; Li, LJ; Li, N; Li, P; Li, T; Li, X; Li, XH; Li, XQ; Li, XX; Li, Y; Li, Z; Li, ZY; Liao, YF; Lin, CC; Lin, MH; Lin, Y; Ling, Y; Links, TP; Lira-Romero, E; Liu, C; Liu, D; Liu, H; Liu, J; Liu, L; Liu, LP; Liu, M; Liu, T; Liu, W; Liu, X; Liu, XH; Liu, Y; Liuwantara, D; Ljumanovic, N; Lobo, L; Lokhande, K; Lopes, A; Lopes, RMRM; López-Gutiérrez, JC; López-Muñoz, MJ; López-Santamaría, M; Lorenzo, C; Lorusso, D; Losito, I; Lu, C; Lu, H; Lu, HZ; Lu, SH; Lu, SN; Lu, Y; Lu, ZY; Luboga, F; Luo, JJ; Luo, KL; Luo, Y; Lutomski, CA; Lv, W; M Piedade, MF; Ma, J; Ma, JQ; Ma, JX; Ma, N; Ma, P; Ma, S; Maciel, M; Madureira, M; Maganaris, C; Maginn, EJ; Mahnashi, MH; Maierhofer, M; Majetschak, M; Malla, TR; Maloney, L; Mann, DL; Mansuri, A; Marelli, E; Margulis, CJ; Marrella, A; Martin, BL; Martín-Francés, L; Martínez de Pinillos, M; Martínez-Navarro, EM; Martinez-Quintanilla Jimenez, D; Martínez-Velasco, A; Martínez-Villaseñor, L; Martinón-Torres, M; Martins, BA; Massongo, M; Mathew, AP; Mathews, D; Matsui, J; Matsumoto, KI; Mau, T; Maves, RC; Mayclin, SJ; Mayer, JM; Maynard, ND; Mayr, T; Mboowa, MG; McEvoy, MP; McIntyre, RC; McKay, JA; McPhail, MJW; McVeigh, AL; Mebazaa, A; Medici, V; Medina, DN; Mehmood, T; Mei-Li, C; Melku, M; Meloncelli, S; Mendes, GC; Mendoza-Velásquez, C; Mercadante, R; Mercado, MI; Merenda, MEZ; Meunier, J; Mi, SL; Michels, M; Mijatovic, V; Mikhailov, V; Milheiro, SA; Miller, DC; Ming, F; Mitsuishi, M; Miyashita, T; Mo, J; Mo, S; Modesto-Mata, M; Moeller, S; Monte, A; Monteiro, L; Montomoli, J; Moore, EE; Moore, HB; Moore, PK; Mor, MK; Moratalla-López, N; Moratilla Lapeña, L; Moreira, R; Moreno, MA; Mörk, AC; Morton, M; Mosier, JM; Mou, LH; Mougharbel, AS; Muccillo-Baisch, AL; Muñoz-Serrano, AJ; Mustafa, B; Nair, GM; Nakanishi, I; Nakanjako, D; Naraparaju, K; Nawani, N; Neffati, R; Neil, EC; Neilipovitz, D; Neira-Borrajo, I; Nelson, MT; Nery, PB; Nese, M; Nguyen, F; Nguyen, MH; Niazy, AA; Nicolaï, J; Nogueira, F; Norbäck, D; Novaretti, JV; O'Donnell, T; O'Dowd, A; O'Malley, DM; Oaknin, A; Ogata, K; Ohkubo, K; Ojha, M; Olaleye, MT; Olawande, B; Olomo, EJ; Ong, EWY; Ono, A; Onwumere, J; Ortiz Bibriesca, DM; Ou, X; Oza, AM; Ozturk, K; Özütemiz, C; Palacio-Pastrana, C; Palaparthi, A; Palevsky, PM; Pan, K; Pantanetti, S; Papachristou, DJ; Pariani, A; Parikh, CR; Parissis, J; Paroul, N; Parry, S; Patel, N; Patel, SM; Patel, VC; Pawar, S; Pefura-Yone, EW; Peixoto Andrade, BCO; Pelepenko, LE; Peña-Lora, D; Peng, S; Pérez-Moro, OS; Perez-Ortiz, AC; Perry, LM; Peter, CM; Phillips, NJ; Phillips, P; Pia Tek, J; Piner, LW; Pinto, EA; Pinto, SN; Piyachaturawat, P; Poka-Mayap, V; Polledri, E; Poloni, TE; Ponessa, G; Poole, ST; Post, AK; Potter, TM; Pressly, BB; Prouty, MG; Prudêncio, M; Pulkki, K; Pupier, C; Qian, H; Qian, ZP; Qiu, Y; Qu, G; Rahimi, S; Rahman, AU; Ramadan, H; Ramanna, S; Ramirez, I; Randolph, GJ; Rasheed, A; Rault, J; Raviprakash, V; Reale, E; Redpath, C; Rema, V; Remucal, CK; Remy, D; Ren, T; Ribeiro, LB; Riboli, G; Richards, J; Rieger, V; Rieusset, J; Riva, A; Rivabella Maknis, T; Robbins, JL; Robinson, CV; Roche-Campo, F; Rodriguez, R; Rodríguez-de-Cía, J; Rollenhagen, JE; Rosen, EP; Rub, D; Rubin, N; Rubin, NT; Ruurda, JP; Saad, O; Sabell, T; Saber, SE; Sabet, M; Sadek, MM; Saejio, A; Salinas, RM; Saliu, IO; Sande, D; Sang, D; Sangenito, LS; Santos, ALSD; Sarmiento Caldas, MC; Sassaroli, S; Sassi, V; Sato, J; Sauaia, A; Saunders, K; Saunders, PR; Savarino, SJ; Scambia, G; Scanlon, N; Schetinger, MR; Schinkel, AFL; Schladweiler, MC; Schofield, CJ; Schuepbach, RA; Schulz, J; Schwartz, N; Scorcella, C; Seeley, J; Seemann, F; Seinige, D; Sengoku, T; Seravalli, J; Sgromo, B; Shaheen, MY; Shan, L; Shanmugam, S; Shao, H; Sharma, S; Shaw, KJ; Shen, BQ; Shen, CH; Shen, P; Shen, S; Shen, Y; Shen, Z; Shi, J; Shi-Li, L; Shimoda, K; Shoji, Y; Shun, C; Silva, MA; Silva-Cardoso, J; Simas, NK; Simirgiotis, MJ; Sincock, SA; Singh, MP; Sionis, A; Siu, J; Sivieri, EM; Sjerps, MJ; Skoczen, SL; Slabon, A; Slette, IJ; Smith, MD; Smith, S; Smith, TG; Snapp, KS; Snow, SJ; Soares, MCF; Soberman, D; Solares, MD; Soliman, I; Song, J; Sorooshian, A; Sorrell, TC; Spinar, J; Staudt, A; Steinhart, C; Stern, ST; Stevens, DM; Stiers, KM; Stimming, U; Su, YG; Subbian, V; Suga, H; Sukhija-Cohen, A; Suksamrarn, A; Suksen, K; Sun, J; Sun, M; Sun, P; Sun, W; Sun, XF; Sun, Y; Sundell, J; Susan, LF; Sutjarit, N; Swamy, KV; Swisher, EM; Sykes, C; Takahashi, JA; Talmor, DS; Tan, B; Tan, ZK; Tang, L; Tang, S; Tanner, JJ; Tanwar, M; Tarazi, Z; Tarvasmäki, T; Tay, FR; Teketel, A; Temitayo, GI; Thersleff, T; Thiessen Philbrook, H; Thompson, LC; Thongon, N; Tian, B; Tian, F; Tian, Q; Timothy, AT; Tingle, MD; Titze, IR; Tolppanen, H; Tong, W; Toyoda, H; Tronconi, L; Tseng, CH; Tu, H; Tu, YJ; Tung, SY; Turpault, S; Tuynman, JB; Uemoto, AT; Ugurlu, M; Ullah, S; Underwood, RS; Ungell, AL; Usandizaga-Elio, I; Vakonakis, I; van Boxel, GI; van den Beucken, JJJP; van der Boom, T; van Slegtenhorst, MA; Vanni, JR; Vaquera, A; Vasconcellos, RS; Velayos, M; Vena, R; Ventura, G; Verso, MG; Vincent, RP; Vitale, F; Vitali, S; Vlek, SL; Vleugels, MPH; Volkmann, N; Vukelic, M; Wagner Mackenzie, B; Wairagala, P; Waller, SB; Wan, J; Wan, MT; Wan, Y; Wang, CC; Wang, H; Wang, J; Wang, JF; Wang, K; Wang, L; Wang, M; Wang, S; Wang, WM; Wang, X; Wang, Y; Wang, YD; Wang, YF; Wang, Z; Wang, ZG; Warriner, K; Weberpals, JI; Weerachayaphorn, J; Wehrli, FW; Wei, J; Wei, KL; Weinheimer, CJ; Weisbord, SD; Wen, S; Wendel Garcia, PD; Williams, JW; Williams, R; Winkler, C; Wirman, AP; Wong, S; Woods, CM; Wu, B; Wu, C; Wu, F; Wu, P; Wu, S; Wu, Y; Wu, YN; Wu, ZH; Wurtzel, JGT; Xia, L; Xia, Z; Xia, ZZ; Xiao, H; Xie, C; Xin, ZM; Xing, Y; Xing, Z; Xu, S; Xu, SB; Xu, T; Xu, X; Xu, Y; Xue, L; Xun, J; Yaffe, MB; Yalew, A; Yamamoto, S; Yan, D; Yan, H; Yan, S; Yan, X; Yang, AD; Yang, E; Yang, H; Yang, J; Yang, JL; Yang, K; Yang, M; Yang, P; Yang, Q; Yang, S; Yang, W; Yang, X; Yang, Y; Yao, JC; Yao, WL; Yao, Y; Yaqub, TB; Ye, J; Ye, W; Yen, CW; Yeter, HH; Yin, C; Yip, V; Yong-Yi, J; Yu, HJ; Yu, MF; Yu, S; Yu, W; Yu, WW; Yu, X; Yuan, P; Yuan, Q; Yue, XY; Zaia, AA; Zakhary, SY; Zalwango, F; Zamalloa, A; Zamparo, P; Zampini, IC; Zani, JL; Zeitoun, R; Zeng, N; Zenteno, JC; Zepeda-Palacio, C; Zhai, C; Zhang, B; Zhang, G; Zhang, J; Zhang, K; Zhang, Q; Zhang, R; Zhang, T; Zhang, X; Zhang, Y; Zhang, YY; Zhao, B; Zhao, D; Zhao, G; Zhao, H; Zhao, Q; Zhao, R; Zhao, S; Zhao, T; Zhao, X; Zhao, XA; Zhao, Y; Zhao, Z; Zheng, Z; Zhi-Min, G; Zhou, CL; Zhou, HD; Zhou, J; Zhou, W; Zhou, XQ; Zhou, Z; Zhu, C; Zhu, H; Zhu, L; Zhu, Y; Zitzmann, N; Zou, L; Zou, Y, 2022
)
0.72
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (3)

RoleDescription
reducing agentThe element or compound in a reduction-oxidation (redox) reaction that donates an electron to another species.
chelatorA ligand with two or more separate binding sites that can bind to a single metallic central atom, forming a chelate.
human metaboliteAny mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
[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 (6)

ClassDescription
1,4-dimercaptobutane-2,3-diolA glycol that is butane-2,3-diol in which a hydrogen from each of the methyl groups is replaced by a thiol group.
dithiol
butanediolsA diol that is a butanediol or a derivative of a butanediol.
glycolA diol in which the two hydroxy groups are on different carbon atoms, usually but not necessarily adjacent.
thiolAn organosulfur compound in which a thiol group, -SH, is attached to a carbon atom of any aliphatic or aromatic moiety.
1,4-dithiothreitolThe threo-diastereomer of 1,4-dimercaptobutane-2,3-diol.
[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 (65)

PathwayProteinsCompounds
Vitamin K Metabolism311
stachyose biosynthesis523
adenine and adenosine salvage II08
purine nucleosides salvage II (plant)419
sinapate ester biosynthesis221
hydroxycinnamate sugar acid ester biosynthesis011
pinitol biosynthesis II016
glucosinolate activation115
saponin biosynthesis II013
hordatine biosynthesis113
lupanine biosynthesis017
4-hydroxybenzoate biosynthesis IV (plants)09
shikonin biosynthesis016
superpathway of carotenoid biosynthesis in plants431
violaxanthin, antheraxanthin and zeaxanthin interconversion59
Renz2020 - GEM of Human alveolar macrophage with SARS-CoV-20490
L-homomethionine biosynthesis420
allantoin degradation to ureidoglycolate II (ammonia producing)518
allantoin degradation to glyoxylate III421
allantoin degradation IV (anaerobic)422
urea cycle633
superpathway of glycolysis and the Entner-Doudoroff pathway2358
superpathway of glycolysis, pyruvate dehydrogenase, TCA, and glyoxylate bypass3989
sanguinarine and macarpine biosynthesis839
CMP-N-acetylneuraminate biosynthesis I (eukaryotes)738
photosynthetic 3-hydroxybutanoate biosynthesis (engineered)6373
pyrimidine deoxyribonucleotides de novo biosynthesis I3034
stachyose biosynthesis323
superpathway of methylglyoxal degradation1330
pyrimidine deoxyribonucleotides de novo biosynthesis III1130
superpathway of L-lysine degradation33112
patchoulol biosynthesis113
geodin biosynthesis020
shikonin biosynthesis017
L-lysine fermentation to acetate and butanoate857
methylglyoxal degradation IV221
superpathway of demethylmenaquinol-8 biosynthesis I1133
parathion degradation213
superpathway of N-acetylneuraminate degradation3979
norspermidine biosynthesis725
hordatine biosynthesis114
superpathway of polyamine biosynthesis III728
histamine biosynthesis421
GDP-mannose biosynthesis1418
superpathway of GDP-mannose-derived O-antigen building blocks biosynthesis1239
superpathway of penicillin, cephalosporin and cephamycin biosynthesis1169
deacetylcephalosporin C biosynthesis444
streptomycin biosynthesis452
gluconeogenesis I2862
superpathway of hexitol degradation (bacteria)2960
ribitol degradation114
adenine and adenosine salvage II415
isopenicillin N biosynthesis323
puromycin biosynthesis227
L-threonine degradation II331
superpathway of L-citrulline metabolism1852
L-citrulline biosynthesis736
superpathway of CMP-sialic acids biosynthesis1460
violaxanthin, antheraxanthin and zeaxanthin interconversion99
alkylnitronates degradation350
superpathway of carotenoid biosynthesis in plants2432
glycolysis II (from fructose 6-phosphate)2149
glycolysis I (from glucose 6-phosphate)3751
2-carboxy-1,4-naphthoquinol biosynthesis2129
superpathway of menaquinol-8 biosynthesis I1036
superpathway of chorismate metabolism56186
ubiquinol-8 biosynthesis (prokaryotic)830
L-ascorbate biosynthesis IV522
superpathway of ubiquinol-8 biosynthesis (prokaryotic)1141
saponin biosynthesis II017
superpathway of L-threonine metabolism2172
superpathway of pentose and pentitol degradation4661

Bioassays (46)

Assay IDTitleYearJournalArticle
AID314742Inhibition of carbonic anhydrase 9 catalytic domain assessed as residual activity at 0.001 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID165312Enzymatic activity of protein tyrosine phosphatase 1B in the presence (10 uM) was measured using para-nitrophenylphosphate (pNPP) as the substrate; active2004Bioorganic & medicinal chemistry letters, Feb-23, Volume: 14, Issue:4
Mechanism of action of pyridazine analogues on protein tyrosine phosphatase 1B (PTP1B).
AID564962Antimicrobial activity against Mycobacterium bovis BCG KOP55 harboring inactivated p55 gene at 5 umol after 14 days by disk diffusion method2009Antimicrobial agents and chemotherapy, Sep, Volume: 53, Issue:9
Role of the Mycobacterium tuberculosis P55 efflux pump in intrinsic drug resistance, oxidative stress responses, and growth.
AID314758Inhibition of carbonic anhydrase 9 assessed as residual activity at 10 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314748Inhibition of carbonic anhydrase 9 catalytic domain assessed as residual activity at 0.1 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID564965Antimicrobial activity against Mycobacterium bovis BCG P55 at 5 umol after 14 days by disk diffusion method2009Antimicrobial agents and chemotherapy, Sep, Volume: 53, Issue:9
Role of the Mycobacterium tuberculosis P55 efflux pump in intrinsic drug resistance, oxidative stress responses, and growth.
AID1281760Induction of apoptosis in Bax deficient human HCT116 cells assessed as early apoptotic cells at 1 mM after 24 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 0.85%)2016European journal of medicinal chemistry, Mar-23, Volume: 111Identification of a new cyathane diterpene that induces mitochondrial and autophagy-dependent apoptosis and shows a potent in vivo anti-colorectal cancer activity.
AID1281733Induction of apoptosis in human HCT116 cells assessed as early apoptotic cells at 1 mM after 24 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 2.2%)2016European journal of medicinal chemistry, Mar-23, Volume: 111Identification of a new cyathane diterpene that induces mitochondrial and autophagy-dependent apoptosis and shows a potent in vivo anti-colorectal cancer activity.
AID314754Inhibition of carbonic anhydrase 9 catalytic domain assessed as residual activity at 2.5 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314746Inhibition of carbonic anhydrase 9 assessed as residual activity at 0.01 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314751Inhibition of carbonic anhydrase 9 catalytic domain assessed as residual activity at 1.0 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314755Inhibition of carbonic anhydrase 9 assessed as residual activity at 2.5 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID1764018Induction of ER stress in human MDA-MB-231 cells assessed as increase in HSPA5A mRNA expression at 2 mM measured after 2 hrs by qPCR method2021Bioorganic & medicinal chemistry letters, 08-15, Volume: 46Synthesis and evaluation of bifunctional PTP4A3 phosphatase inhibitors activating the ER stress pathway.
AID314745Inhibition of carbonic anhydrase 9 catalytic domain assessed as residual activity at 0.01 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID1281763Induction of apoptosis in Bax deficient human HCT116 cells assessed as late apoptotic cells at 1 mM after 24 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 1.56%)2016European journal of medicinal chemistry, Mar-23, Volume: 111Identification of a new cyathane diterpene that induces mitochondrial and autophagy-dependent apoptosis and shows a potent in vivo anti-colorectal cancer activity.
AID314753Inhibition of carbonic anhydrase 2 assessed as residual activity at 2.5 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314741Inhibition of carbonic anhydrase 2 assessed as residual activity at 0.001 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID159829Dithiothreitol (10 nM) reactivation of human placental aromatase following 1.0 uM inactivation for 10 minutes1989Journal of medicinal chemistry, Jan, Volume: 32, Issue:1
Interactions of thiol-containing androgens with human placental aromatase.
AID314743Inhibition of carbonic anhydrase 9 assessed as residual activity at 0.001 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314752Inhibition of carbonic anhydrase 9 assessed as residual activity at 1.0 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID1281740Induction of apoptosis in human HCT116 cells assessed as necrotic cells at 1 mM after 24 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 0.44%)2016European journal of medicinal chemistry, Mar-23, Volume: 111Identification of a new cyathane diterpene that induces mitochondrial and autophagy-dependent apoptosis and shows a potent in vivo anti-colorectal cancer activity.
AID314756Inhibition of carbonic anhydrase 2 assessed as residual activity at 10 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID1764026Induction of ER stress in human MDA-MB-231 cells assessed as increase in sXbp1 mRNA expression at 2 mM measured after 2 hrs by qPCR method2021Bioorganic & medicinal chemistry letters, 08-15, Volume: 46Synthesis and evaluation of bifunctional PTP4A3 phosphatase inhibitors activating the ER stress pathway.
AID1281736Induction of apoptosis in human HCT116 cells assessed as late apoptotic cells at 1 mM after 24 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 3.73%)2016European journal of medicinal chemistry, Mar-23, Volume: 111Identification of a new cyathane diterpene that induces mitochondrial and autophagy-dependent apoptosis and shows a potent in vivo anti-colorectal cancer activity.
AID159830Dithiothreitol (10 nM) reactivation of human placental aromatase following 1.0 uM inactivation for 5 minutes1989Journal of medicinal chemistry, Jan, Volume: 32, Issue:1
Interactions of thiol-containing androgens with human placental aromatase.
AID314744Inhibition of carbonic anhydrase 2 assessed as residual activity at 0.01 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314747Inhibition of carbonic anhydrase 2 assessed as residual activity at 0.1 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314749Inhibition of carbonic anhydrase 9 assessed as residual activity at 0.1 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID1281730Induction of apoptosis in human HCT116 cells assessed as viable cells at 1 mM after 24 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 93.64%)2016European journal of medicinal chemistry, Mar-23, Volume: 111Identification of a new cyathane diterpene that induces mitochondrial and autophagy-dependent apoptosis and shows a potent in vivo anti-colorectal cancer activity.
AID1764027Induction of ER stress in human MDA-MB-231 cells assessed as increase in DDIT3 mRNA expression at 2 mM measured after 2 hrs by qPCR method2021Bioorganic & medicinal chemistry letters, 08-15, Volume: 46Synthesis and evaluation of bifunctional PTP4A3 phosphatase inhibitors activating the ER stress pathway.
AID314750Inhibition of carbonic anhydrase 2 assessed as residual activity at 1.0 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID314757Inhibition of carbonic anhydrase 9 catalytic domain assessed as residual activity at 10 mM2008Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6
Carbonic anhydrase inhibitors: the very weak inhibitors dithiothreitol, beta-mercaptoethanol, tris(carboxyethyl)phosphine and threitol interfere with the binding of sulfonamides to isozymes II and IX.
AID637281Dissociation constant, pKa of the compound2012Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2
Oxidative folding of lysozyme with aromatic dithiols, and aliphatic and aromatic monothiols.
AID534106Antibacterial activity against Pasteurella multocida AL435 after 24 hrs by broth dilution method2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID534111Antibacterial activity against Pasteurella multocida pm1980 after 24 hrs by broth dilution method2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID699332Inhibition of human activated TAFI using Hip-Arg as substrate at 10 uM incubated for 10 mins prior to substrate addition measured after 30 mins by spectrophotometric analysis2012Journal of medicinal chemistry, Sep-13, Volume: 55, Issue:17
Design and characterization of a selenium-containing inhibitor of activated thrombin-activatable fibrinolysis inhibitor (TAFIa), a zinc-containing metalloprotease.
AID534107Antibacterial activity against TolC deficient Pasteurella multocida pm0527 after 24 hrs by broth dilution method2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID657488Inhibition of desert banana tyrosinase using p-cresol as substrate2012Bioorganic & medicinal chemistry, May-01, Volume: 20, Issue:9
New saccharin derivatives as tyrosinase inhibitors.
AID695851Resistance index, ratio of IC50 for human KB-3-1 cells to IC50 for drug-resistant human KBV1 cells expressing P-gp2011Journal of medicinal chemistry, Jul-28, Volume: 54, Issue:14
Collateral sensitivity of multidrug-resistant cells to the orphan drug tiopronin.
AID534109Ratio of MIC for Pasteurella multocida AL435 to MIC for TolC deficient Pasteurella multocida pm05272008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID534112Ratio of MIC for Pasteurella multocida AL435 to MIC for TolC deficient Pasteurella multocida pm19802008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID695876Cytotoxicity against drug-resistant human KBV1 cells expressing P-gp incubated for 72 hrs by MTT assay2011Journal of medicinal chemistry, Jul-28, Volume: 54, Issue:14
Collateral sensitivity of multidrug-resistant cells to the orphan drug tiopronin.
AID322756Inhibition of HSV1 entry in african green monkey Vero cells assessed as beta-galactosidase activity relative to control by ELISA2007Antimicrobial agents and chemotherapy, May, Volume: 51, Issue:5
Addition of a C-terminal cysteine improves the anti-herpes simplex virus activity of a peptide containing the human immunodeficiency virus type 1 TAT protein transduction domain.
AID534110Antibacterial activity against TolC deficient Pasteurella multocida pm1980 after 24 hrs by broth dilution method2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID534108Antibacterial activity against Pasteurella multocida pm0527 after 24 hrs by broth dilution method2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Characterization of TolC efflux pump proteins from Pasteurella multocida.
AID695877Cytotoxicity against human KB-3-1 cells incubated for 72 hrs by MTT assay2011Journal of medicinal chemistry, Jul-28, Volume: 54, Issue:14
Collateral sensitivity of multidrug-resistant cells to the orphan drug tiopronin.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (7,338)

TimeframeStudies, This Drug (%)All Drugs %
pre-19903174 (43.25)18.7374
1990's1940 (26.44)18.2507
2000's1365 (18.60)29.6817
2010's751 (10.23)24.3611
2020's108 (1.47)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 70.19

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 Index70.19 (24.57)
Research Supply Index8.93 (2.92)
Research Growth Index4.28 (4.65)
Search Engine Demand Index127.83 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (70.19)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials12 (0.16%)5.53%
Trials0 (0.00%)5.53%
Reviews47 (0.62%)6.00%
Reviews0 (0.00%)6.00%
Case Studies26 (0.35%)4.05%
Case Studies0 (0.00%)4.05%
Observational4 (0.05%)0.25%
Observational0 (0.00%)0.25%
Other7,445 (98.82%)84.16%
Other6 (100.00%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]