|
In vitro inhibition against 5-lipoxygenase in RBL-1 cells was determined at 10e-4 M
|
None
|
-0.1
%
|
|
|
In vitro inhibition of rabbit lens aldose reductase at 10e-4 M.
|
Oryctolagus cuniculus
|
50.0
%
|
|
|
In vitro inhibition of rabbit lens aldose reductase at 10e-5 M.
|
Oryctolagus cuniculus
|
15.0
%
|
|
|
In vitro inhibition of rabbit lens aldose reductase at 10e-6 M.
|
Oryctolagus cuniculus
|
5.0
%
|
|
|
Compound is evaluated for the inhibition of [125I]T3 uptake by H4 rat hepatoma cells at 0.1 mM
|
Rattus norvegicus
|
64.4
%
|
|
|
Inhibition of binding of Batrachotoxinin [3H]BTX-B to high affinity sites on voltage dependent sodium channels in a vesicular preparation from guinea pig cerebral cortex at 10 uM
|
Cavia porcellus
|
26.7
%
|
|
|
Inhibition of LDL oxidation at 5 uM by ELISA
|
None
|
97.0
%
|
|
|
Inhibition of LDL oxidation at 15 uM by ELISA
|
None
|
82.0
%
|
|
|
Inhibition of LDL oxidation at 30 uM by ELISA
|
None
|
23.0
%
|
|
|
Inhibition of LDL oxidation at 300 uM by ELISA
|
None
|
10.0
%
|
|
|
Inhibition of chlorinating activity of recombinant myeloperoxidase at 0.5 uM by taurine assay
|
None
|
25.0
%
|
|
|
Inhibition of chlorinating activity of recombinant myeloperoxidase at 1 uM by taurine assay
|
None
|
40.0
%
|
|
|
Inhibition of chlorinating activity of recombinant myeloperoxidase at 2 uM by taurine assay
|
None
|
52.0
%
|
|
|
Inhibition of chlorinating activity of recombinant myeloperoxidase at 4 uM by taurine assay
|
None
|
64.0
%
|
|
|
Activity at androgen receptor ligand binding domain assessed as inhibition of SRC2-3 interaction at 50 uM after 2 hrs by fluorescence polarization assay
|
None
|
42.0
%
|
|
|
Inhibition of AKR1C3 by fluorimetric method
|
None
|
51.0
nM
|
|
|
Inhibition of AKR1C2 by fluorimetric method
|
None
|
370.0
nM
|
|
|
Inhibition of recombinant COX2
|
None
|
20.0
nM
|
|
|
Inhibition of recombinant AKR1C3 assessed as NADP+ dependent oxidation of S-tetralol by fluorescence assay
|
None
|
50.0
nM
|
|
|
Inhibition of recombinant AKR1C2 assessed as NADP+ dependent oxidation of S-tetralol by fluorescence assay
|
None
|
370.0
nM
|
|
|
Inhibition of COX2 expressed in baculovirus infected SF-21 cells assessed as formation of PGH2 from PGG2 using arachidonic acid as substrate preincubated for 5 mins
|
None
|
16.0
nM
|
|
|
Inhibition of human recombinant N-terminal His6-tagged AKR1C3 expressed in Escherichia coli BL21(DE3) cells using 8-Acetyl-2,3,5,6-tetrahydro-1H,4H-11-oxa-3a-aza-benzo[de]anthracen-10-one as substrate after 1 hr by fluorimetric analysis
|
Homo sapiens
|
410.0
nM
|
|
|
Inhibition of AKR1C3 (unknown origin)
|
Homo sapiens
|
410.0
nM
|
|
|
Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM
|
Cricetulus griseus
|
211.28
%
|
|
|
Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM
|
Cricetulus griseus
|
64.03
%
|
|
|
Binding affinity to human recombinant TTR Y78F mutant after 5 mins by isothermal titration calorimetry
|
Homo sapiens
|
109.0
nM
|
|
|
Inhibition of human recombinant TTR Y78F mutant-mediated fibrillogenesis at 40 uM after 30 mins by turbidimetric assay relative to control
|
Homo sapiens
|
89.0
%
|
|
|
Inhibition of wild-type N-terminal 6-His tagged AKR1B10 (unknown origin) expressed in Escherichia coli BL21(DE3) assessed as pyridine-3-aldehyde reduction by spectrophotometry
|
Homo sapiens
|
760.0
nM
|
|
|
Antiinflammatory activity in rat assessed as reduction of carrageenan-induced paw oedema at 0.15 mmol/kg, ip administered 5 mins before carrageenan challenge measured after 3.5 hrs
|
Rattus norvegicus
|
19.0
%
|
|
|
Inhibition of recombinant human N-terminal His6-tagged AKR1B10 expressed in Escherichia coli BL21 (DE3) pLysS cells by pyridine-3-aldehyde reductase activity assay
|
Homo sapiens
|
760.0
nM
|
|
|
Anti-inflammatory activity in rat assessed as reduction of carrageenan-induced paw edema at 150 umol/kg, ip after 3.5 hrs relative to control
|
Rattus norvegicus
|
19.0
%
|
|
|
Discontinuous Radiometric Assay: Compounds may be evaluated as selective reversible inhibitors of AKR1C3 by screening them against homogeneous recombinant AKR1C1-AKR1C4 expressed in E. coli. In each case, a discontinuous radiometric assay may be used to monitor the inhibition of progesterone reduction (20-ketosteroid reduction) catalyzed by AKR1C1, the inhibition of Δ4-AD reduction (17-ketosteroid reduction) catalyzed by AKR1C3, and the inhibition of 5α-DHT reduction (3-ketosteroid reduction) catalyzed by AKR1C2 and AKR1C4 (by measuring the formation of 20α-hydroxyprogesterone, testosterone or 3α-androstanediol by radiochromatography). Secondary screens of the compounds of interest include: (a) a full-screen against all nine human recombinant AKR enzymes to ensure there are no-intended off-target effects (in this context AKR1B10 (retinal reductase; SEQ ID NO:5) has been shown to be potently inhibited by N-phenylanthranilates) (Endo et al., 2010, Biol. Pharm. Bull. 33:886-90); (b) a screen against COX-1 and COX-2 to reaffirm that compounds do not act as NSAIDs; and (c) an expanded screen against other nuclear receptors (especially other steroid hormone receptors).
|
Homo sapiens
|
51.0
nM
|
|
|
Discontinuous Radiometric Assay: Compounds may be evaluated as selective reversible inhibitors of AKR1C3 by screening them against homogeneous recombinant AKR1C1-AKR1C4 expressed in E. coli. In each case, a discontinuous radiometric assay may be used to monitor the inhibition of progesterone reduction (20-ketosteroid reduction) catalyzed by AKR1C1, the inhibition of Δ4-AD reduction (17-ketosteroid reduction) catalyzed by AKR1C3, and the inhibition of 5α-DHT reduction (3-ketosteroid reduction) catalyzed by AKR1C2 and AKR1C4 (by measuring the formation of 20α-hydroxyprogesterone, testosterone or 3α-androstanediol by radiochromatography). Secondary screens of the compounds of interest include: (a) a full-screen against all nine human recombinant AKR enzymes to ensure there are no-intended off-target effects (in this context AKR1B10 (retinal reductase; SEQ ID NO:5) has been shown to be potently inhibited by N-phenylanthranilates) (Endo et al., 2010, Biol. Pharm. Bull. 33:886-90); (b) a screen against COX-1 and COX-2 to reaffirm that compounds do not act as NSAIDs; and (c) an expanded screen against other nuclear receptors (especially other steroid hormone receptors).
|
Homo sapiens
|
630.0
nM
|
|
Discontinuous Radiometric Assay: Compounds may be evaluated as selective reversible inhibitors of AKR1C3 by screening them against homogeneous recombinant AKR1C1-AKR1C4 expressed in E. coli. In each case, a discontinuous radiometric assay may be used to monitor the inhibition of progesterone reduction (20-ketosteroid reduction) catalyzed by AKR1C1, the inhibition of Δ4-AD reduction (17-ketosteroid reduction) catalyzed by AKR1C3, and the inhibition of 5α-DHT reduction (3-ketosteroid reduction) catalyzed by AKR1C2 and AKR1C4 (by measuring the formation of 20α-hydroxyprogesterone, testosterone or 3α-androstanediol by radiochromatography). Secondary screens of the compounds of interest include: (a) a full-screen against all nine human recombinant AKR enzymes to ensure there are no-intended off-target effects (in this context AKR1B10 (retinal reductase; SEQ ID NO:5) has been shown to be potently inhibited by N-phenylanthranilates) (Endo et al., 2010, Biol. Pharm. Bull. 33:886-90); (b) a screen against COX-1 and COX-2 to reaffirm that compounds do not act as NSAIDs; and (c) an expanded screen against other nuclear receptors (especially other steroid hormone receptors).
|
Homo sapiens
|
370.0
nM
|
|
|
Discontinuous Radiometric Assay: Compounds may be evaluated as selective reversible inhibitors of AKR1C3 by screening them against homogeneous recombinant AKR1C1-AKR1C4 expressed in E. coli. In each case, a discontinuous radiometric assay may be used to monitor the inhibition of progesterone reduction (20-ketosteroid reduction) catalyzed by AKR1C1, the inhibition of Δ4-AD reduction (17-ketosteroid reduction) catalyzed by AKR1C3, and the inhibition of 5α-DHT reduction (3-ketosteroid reduction) catalyzed by AKR1C2 and AKR1C4 (by measuring the formation of 20α-hydroxyprogesterone, testosterone or 3α-androstanediol by radiochromatography). Secondary screens of the compounds of interest include: (a) a full-screen against all nine human recombinant AKR enzymes to ensure there are no-intended off-target effects (in this context AKR1B10 (retinal reductase; SEQ ID NO:5) has been shown to be potently inhibited by N-phenylanthranilates) (Endo et al., 2010, Biol. Pharm. Bull. 33:886-90); (b) a screen against COX-1 and COX-2 to reaffirm that compounds do not act as NSAIDs; and (c) an expanded screen against other nuclear receptors (especially other steroid hormone receptors).
|
Homo sapiens
|
980.0
nM
|
|
|
Discontinuous Radiometric Assay: Compounds may be evaluated as selective reversible inhibitors of AKR1C3 by screening them against homogeneous recombinant AKR1C1-AKR1C4 expressed in E. coli. In each case, a discontinuous radiometric assay may be used to monitor the inhibition of progesterone reduction (20-ketosteroid reduction) catalyzed by AKR1C1, the inhibition of Δ4-AD reduction (17-ketosteroid reduction) catalyzed by AKR1C3, and the inhibition of 5α-DHT reduction (3-ketosteroid reduction) catalyzed by AKR1C2 and AKR1C4 (by measuring the formation of 20α-hydroxyprogesterone, testosterone or 3α-androstanediol by radiochromatography). Secondary screens of the compounds of interest include: (a) a full-screen against all nine human recombinant AKR enzymes to ensure there are no-intended off-target effects (in this context AKR1B10 (retinal reductase; SEQ ID NO:5) has been shown to be potently inhibited by N-phenylanthranilates) (Endo et al., 2010, Biol. Pharm. Bull. 33:886-90); (b) a screen against COX-1 and COX-2 to reaffirm that compounds do not act as NSAIDs; and (c) an expanded screen against other nuclear receptors (especially other steroid hormone receptors).
|
Homo sapiens
|
16.0
nM
|
|
|
Inhibition of acid-induced wild type transthyretin (unknown origin) aggregation expressed in Escherichia coli pre-incubated for 30 mins before acid addition and further incubated for 72 hrs at 37 degC under dark conditions by UV-Vis spectrophotometry
|
Homo sapiens
|
98.0
%
|
|
|
Inhibition of AKR1C3 (unknown origin) using S-tetralol as substrate in presence of NADP+ by fluorimtery
|
Homo sapiens
|
440.0
nM
|
|
|
Inhibition of AKR1C2 (unknown origin) using S-tetralol as substrate by by fluorimtery
|
Homo sapiens
|
530.0
nM
|
|
|
Inhibition of human COX2 assessed as reduction in PGF2alpha production at 100 uM by ELISA
|
Homo sapiens
|
18.0
%
|
|
|
Inhibition of recombinant N-terminal GST-tagged human AKR1C3 expressed in Escherichia coli BL21 (DE) Codon Plus RP cells using S-tetralol as substrate in presence of NADP+ by fluorimetric analysis
|
Homo sapiens
|
440.0
nM
|
|
|
Inhibition of recombinant N-terminal GST-tagged human AKR1C2 expressed in Escherichia coli BL21 (DE) Codon Plus RP cells using S-tetralol as substrate in presence of NADP+ by fluorimetric analysis
|
Homo sapiens
|
530.0
nM
|
|
|
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells at 10 uM after 48 hours by high content imaging
|
Homo sapiens
|
-0.17
%
|
|
|
Inhibition of NAPRT (unknown origin)
|
Homo sapiens
|
0.01
nM
|
|
|
Inhibition of human recombinant AKR1C2-mediated reduction of [3H]5alpha-DHT at 10 uM
|
Homo sapiens
|
70.0
%
|
|
|
SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate
|
Severe acute respiratory syndrome coronavirus 2
|
6.16
%
|
|
SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate
|
Severe acute respiratory syndrome coronavirus 2
|
29.44
%
|
|
|
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging
|
Chlorocebus sabaeus
|
0.06
%
|
|
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging
|
Chlorocebus sabaeus
|
-0.04
%
|
|
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging
|
Chlorocebus sabaeus
|
-0.04
%
|
|
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging
|
Chlorocebus sabaeus
|
0.06
%
|
|
|
Binding affinity to wild type TTR (unknown origin) expressed in Escherichia coli BL21/DE3 by Circular dichroism spectroscopy
|
Homo sapiens
|
30.0
nM
|
|
