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(2R,3R,4S,5R)-2-(3,4-dichlorophenyl)-4-(hexylsulfanyl)-1-[(4-methylphenyl)sulfonyl]-5-propylpyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-2-(4-bromophenyl)-1-[(4-methylphenyl)sulfonyl]-4-(pentylsulfanyl)-5-propylpyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-2-(4-bromophenyl)-4-(hexylsulfanyl)-1-[(4-methylphenyl)sulfonyl]-5-propylpyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-2-(4-bromophenyl)-4-[(4-methoxyphenyl)sulfanyl]-1-[(4-methylphenyl)sulfonyl]-5-propylpyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-2-(4-bromophenyl)-5-ethyl-4-(hexylsulfanyl)-1-[(4-methylphenyl)sulfonyl]pyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-2-(4-bromophenyl)-5-hexyl-4-(hexylsulfanyl)-1-[(4-methylphenyl)sulfonyl]pyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-4-[(3-tert-butoxy-3-oxopropyl)sulfanyl]-2-(3-chlorophenyl)-5-(cyclopentylmethyl)-1-[(4-methylphenyl)sulfonyl]pyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-4-[(3-tert-butoxy-3-oxopropyl)sulfanyl]-2-(4-chlorophenyl)-1-[(4-chlorophenyl)sulfonyl]-5-(cyclopentylmethyl)pyrrolidine-3-carboxylic acid
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(2R,3R,4S,5R)-4-[(3-tert-butoxy-3-oxopropyl)sulfanyl]-2-(4-chlorophenyl)-5-(cyclopentylmethyl)-1-(phenylsulfonyl)pyrrolidine-3-carboxylic acid
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(2R,3R,5S)-5-tert-butyl-2-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]pyrrolidine-3-carboxylic acid
compete with the substrate protein rather than GGPP; compete with the substrate protein rather than GGPP
(2S,5R)-5-ethyl-2-(4-fluorophenyl)-1-tosyl-2,5-dihydro-1H-pyrrole-3-carboxylic acid
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IC50: 0.2 mM using RhoA as a substrate, IC50: 0.25 mM using Ki-Ras4B as a substrate
(2S,5S)-5-tert-butyl-2-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-2,5-dihydro-1H-pyrrole-3-carboxylic acid
(2S,6S)-2,6-bis(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-1,2,5,6-tetrahydropyridine-3-carboxylic acid
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IC50: 0.0003 mM using RhoA as a substrate, IC50: 0.002 mM using Ki-Ras4B as a substrate
(2S,6S)-6-(4-fluorophenyl)-1-[(4-methylphenyl)sulfonyl]-2-phenyl-1,2,5,6-tetrahydropyridine-3-carboxylic acid
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IC50: 0.12 mM using RhoA as a substrate, IC50: 0.08 mM using Ki-Ras4B as a substrate
(S)-N-(1-amino-3-(4-fluorophenyl)-1-oxopropan-2-yl)-4-((1-(3,4-dichlorophenyl)-4-(2-(methylthio)ethyl)-3-(pyridin-3-yl)-1H-pyrazol-5-yl)oxy)butanamide
potent GGT1 inhibitor, anti-proliferative efficacy against MDA-MB-231 cells has an IC50 value of 0.0076 mM
(S)-N-(1-amino-3-(4-methoxyphenyl)-1-oxopropan-2-yl)-4-((1-(3,4-dichlorophenyl)-4-(2-(methylthio)ethyl)-3-(pyridin-3-yl)-1H-pyrazol-5-yl)oxy)butanamide
potent GGT1 inhibitor
(S)-N-(4-(3,4-dichlorophenoxy)benzyl)-6-(1H-indol-3-yl)piperazine-2,5-dione
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dual inhibitor for both farnesyl transferase and geranygeranyltransferase-I. Compound occupies both isoprenoid and peptide substrate binding sites
(S)-N-(4-(3-chlorophenoxy)benzyl)-6-(1H-indol-3-yl)piperazine-2,5-dione
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dual inhibitor for both farnesyl transferase and geranygeranyltransferase-I
1-phosphono-(E,E,E)-geranylgeraniol
1-[2-[(Z)-[[4-(8-chloro-10,11-dihydrodibenzo[b,f]thiepin-10-yl)piperazin-1-yl]imino]methyl]phenoxy]-N,N-dimethylmethanamine
i.e L-269289, selective chemical inhibition of GGTase I by L-269289 potentiates echinocandin activity and renders echinocandin-resistant Candida albicans responsive to treatment in vitro and in animal models for disseminated infection
1-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-cyclohexanecarboxylic acid
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IC50: 6525 nM
1-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-cyclohexanecarboxylic acid methyl ester
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IC50: above 0.01 mM
11-aminoundecylcarbonyl-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine
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competitive. bivalent inhibitor for simultaneous recognition of both exteriorand interior protein surface. Not inhibitory against farnesyltransferase
2-(3-chlorophenyl)-6-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-1,2,5,6-tetrahydropyridine-3-carboxylic acid
compete with the substrate protein rather than GGPP; compete with the substrate protein rather than GGPP
2-aryl-4-aminobenzoic acid
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IC50: 21 nM
2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-N-(3-methyl-butyl)-acetamide
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IC50: above 0.01 mM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl] acetylamino}-4-methyl-pentanoic acid methyl ester
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IC50: above 0.01 mM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-3-phenyl-propionic acid
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IC50: 0.0063 mM; IC50: 170 nM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-3-phenyl-propionic acid methyl ester
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IC50: 4500 nM; IC50: above 0.01 mM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-4-methyl-pentanoic acid
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IC50: 2700 nM; IC50: 580 nM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-4-methyl-pentanoic acid methyl ester
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IC50: above 0.01 mM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-4-methylsulfanyl-butyric acid
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IC50: 3350 nM
2-{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-4-methylsulfanyl-butyric acid methyl ester
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IC50: above 0.01 mM
3-(4'-farnesyloxy-3'-methoxyphenyl)-2-trans propenoic acid
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0.1 mM, 83.9% inhibition
3-(4'-farnesyloxy-3'-OH-phenyl)-2-trans propenoic acid
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0.1 mM, 93.5% inhibition
3-(4'-geranyloxy-3'-methoxyphenyl)-2-trans propenoic acid
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0.1 mM, 78.6% inhibition
3-(4'-geranyloxy-3'-methoxyphenyl)-2-trans propenoic acid ethyl ester
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0.1 mM, 3% inhibition
3-(4'-geranyloxy-3'-OH-phenyl)-2-trans propenoic acid
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0.1 mM, 72.4% inhibition
3-(4'-geranyloxy-3'-OH-phenyl)-2-trans propenoic acid ethyl ester
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0.1 mM, 7.5% inhibition
3-(4'-isopentenyloxy-3'-OH-phenyl)-2-trans propenoic acid
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0.1 mM, 46.4% inhibition
3-aza-geranylgeranyl-diphosphate
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competitive inhibitor with respect to geranylgeranyl diphosphate, non-competitive to Cys-Val-Phe-Leu
3-chloro-N-[2-oxo-2-[2-[[1-phenyl-3-(4-propoxyphenyl)pyrazol-4-yl]methylidene]hydrazinyl]ethyl]benzamide
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GGTI-DU.Sig1, PubChem CID 3311883, inhibitor of protein geranylgeranyltransferase type I
4-[2-[4-(3-chlorophenyl)-3-oxopiperazin-1-yl]-2-(1H-imidazol-5-yl)ethyl]benzonitrile
is bound to the peptide-binding site by competing with the CAAX substrate in the 4-[2-[4-(3-chlorophenyl)-3-oxopiperazin-1-yl]-2-(1H-imidazol-5-yl)ethyl]benzonitrile-FTase complex, cf. EC 2.5.1.58, but is bound in the lipid-binding pocket together with a portion of the peptide-binding site in the 4-[2-[4-(3-chlorophenyl)-3-oxopiperazin-1-yl]-2-(1H-imidazol-5-yl)ethyl]benzonitrile-GGTase-I complex; is bound to the peptide-binding site by competing with the CAAX substrate in the 4-[2-[4-(3-chlorophenyl)-3-oxopiperazin-1-yl]-2-(1H-imidazol-5-yl)ethyl]benzonitrileFTase complex, cf. EC 2.5.1.58, but is bound in the lipid-binding pocket together with a portion of the peptide-binding site in the L-4-[2-[4-(3-chlorophenyl)-3-oxopiperazin-1-yl]-2-(1H-imidazol-5-yl)ethyl]benzonitrile-GGTase-I complex
4-[[([5-[(4-ethylphenoxy)methyl]-4-(1-phenylethyl)-4H-pyrazol-3-yl]sulfanyl)acetyl]amino]benzamide
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inhibitor identified using quantitative structure-activity realtionship models and virtual screening of chemicals. confirmation of predicted data by experiment
4-[[2-[[5-(2-methoxyphenyl)-4-phenethyl-1,2,4-triazol-3-yl]sulfanyl]acetyl]amino]benzamide
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GGTI-DU.En1, PubChem CID 2118978, inhibitor of protein geranylgeranyltransferase type I
4-[[2-[[5-[(4-ethylphenoxy)methyl]-4-(1-phenylethyl)-1,2,4-triazol-3-yl]sulfanyl]acetyl]amino]benzamide
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GGTI-DU.En2, PubChem CID 3455185, inhibitor of protein geranylgeranyltransferase type I, no or little activity against protein farnesyltransferase
auraptene
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0.1 mM, 18.6% inhibition
boropinic acid
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0.1 mM, 31% inhibition
collinin
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0.1 mM, 34.2% inhibition
Cys-3-(aminomethyl)benzoic acid-Leu
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noncompetitive to geranylgeranyl diphosphate, competitive to dansyl-Gly-Cys-Ile-Ile-Leu
Cys-Val-Phe-Leu
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noncompetitive inhibitor with respect to geranylgeranyl diphosphate, 50% inhibition at 0.0001 mM, competitive to Cys-Val-Phe-Leu
diethyl dicarbonate
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80% loss of activity at 5 mM
GGTI-2151
16.3% inhibition at 50 nM
GGTI-2154
14.7% inhibition at 50 nM
GGTI-2418
a GGTI inhibitor, in clinical trials as potential anti-tumor agent in breast cancer; a GGTI inhibitor, in clinical trials as potential anti-tumor agent in breast cancer
L-cysteinyl-L-valyl-L-isoleucyl-L-leucine
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manumycin A
the cdc43DELTA mutant is 2fold more susceptible to this farnesyltransferase inhibitor than the wild-type
methyl N-([2-(3-chlorophenyl)-6-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-1,2,5,6-tetrahydropyridin-3-yl]carbonyl)leucinate
with anti-tumor activity; with anti-tumor activity
N-(12-ammoniododecanoyl)-D-cysteinyl-L-valyl-L-isoleucyl-L-leucine trifluoroacetate
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N-(12-[[(3-[[(3R)-3-ammonio-4-phenylbutyl]oxy]-4,5-bis[[(3S)-3-ammonio-4-phenylbutyl]oxy]phenyl)carbonyl]amino]dodecanoyl)-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine tris(trifluoroacetate)
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N-(2,5-dichlorophenyl)-N'-[[3-(4-methylphenyl)-1-phenylpyrazol-4-yl]methylideneamino]oxamide
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GGTI-DU.Sig2, PubChem CID 4277701, inhibitor of protein geranylgeranyltransferase type I
N-(4-[[(3-[[(3R)-3-ammonio-4-phenylbutyl]oxy]-4,5-bis[[(3S)-3-ammonio-4-phenylbutyl]oxy]phenyl)carbonyl]amino]butanoyl)-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine tris(trifluoroacetate)
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N-([(2S)-2-benzyl-4-[(4-methyl-1H-imidazol-5-yl)methyl]-3-oxopiperazin-1-yl]carbonyl)-L-leucine
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N-([5-[(1H-imidazol-5-ylamino)methyl]-2'-methylbiphenyl-2-yl]carbonyl)-L-leucine
a non-thiol-containing peptidomi-metic, it can inhibit human tumor growth in mice and the combination therapy with cytotoxic agents is more beneficial than monotherapy. N-([5-[(1H-imidazol-5-ylamino)methyl]-2'-methylbiphenyl-2-yl]carbonyl)-L-leucine is able to induce breast carcinoma apoptosis and tumor regression in H-Ras transgenic mice; a non-thiol-containing peptidomi-metic, it can inhibit human tumor growth in mice and the combination therapy with cytotoxic agents is more beneficial than monotherapy. N-([5-[(1H-imidazol-5-ylamino)methyl]-2'-methylbiphenyl-2-yl]carbonyl)-L-leucine is able to induce breast carcinoma apoptosis and tumor regression in H-Ras transgenic mice
N-benzyl-2-[(2-chlorobenzyl)[[5-(4-methylphenyl)-2H-tetrazol-2-yl]acetyl]amino]butanamide
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inhibitor identified using quantitative structure-activity realtionship models and virtual screening of chemicals. confirmation of predicted data by experiment
N-benzyl-2-[(2-chlorophenyl)methyl-[2-[5-(4-methylphenyl)tetrazol-2-yl]acetyl]amino]butanamide
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GGTI-DU.As2, PubChem CID 3180738, inhibitor of protein geranylgeranyltransferase type I, no or little activity against protein farnesyltransferase
N-[(5-[[(2R)-2-amino-3-sulfanylpropyl]amino]biphenyl-2-yl)carbonyl]-L-leucine
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N-[(E)-1-(benzylcarbamoyl)-2-[5-(3,4-dichlorophenyl)furan-2-yl]ethenyl]-4-methylbenzamide
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inhibitor identified using quantitative structure-activity realtionship models and virtual screening of chemicals. confirmation of predicted data by experiment
N-[12-([[3,4,5-tris(3-ammoniopropoxy)phenyl]carbonyl]amino)dodecanoyl]-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine tris(trifluoroacetate)
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N-[2-(benzylamino)-2-oxoethyl]-2-[5-(4-chlorophenyl)tetrazol-2-yl]-N-(4-propan-2-ylphenyl)acetamide
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GGTI-DU.As1, PubChem CID 3180720, inhibitor of protein geranylgeranyltransferase type I
N-[3-(benzylamino)-1-[5-(3,4-dichlorophenyl)furan-2-yl]-3-oxoprop-1-en-2-yl]-4-methylbenzamide
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GGTI-DU.Sig3, PubChem CID 5143450, inhibitor of protein geranylgeranyltransferase type I, no or little activity against protein farnesyltransferase
N-[6-(3,4,5-tris(3-amino-1-propoxy)benzoylamino)-undecylcarbonyl]-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine
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competitive, bivalent inhibitor for simultaneous recognition of both exterior and interior protein surface. Not inhibitory against farnesyltransferase
N-[6-(3,4,5-tris(3-amino-4-phenyl-1-butoxy)benzoylamino)-hexylcarbonyl]-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine trifluoroacetate
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-
N-[6-(3,4,5-tris(3-amino-4-phenyl-1-butoxy)benzoylamino)-propylcarbonyl]-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine
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bivalent inhibitor for simultaneous recognition of both exterior and interior protein surface. Not inhibitory against farnesyltransferase
N-[6-(3,4,5-tris(3-amino-4-phenyl-1-butoxy)benzoylamino)-undecylcarbonyl]-L-cysteinyl-L-valyl-L-isoleucyl-L-leucine
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competitive, bivalent inhibitor for simultaneous recognition of both exterior and interior protein surface. Not inhibitory against farnesyltransferase
N-[[4-(imidazol-4-yl)methylamino]-2-(1-naphthyl)benzoyl]leucine
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Na-(4-[[1-(3,4-dichlorophenyl)-4-[2-(methylsulfanyl)ethyl]-3-(pyridin-3-yl)-1H-pyrazol-5-yl]oxy]butanoyl)-L-phenylalaninamide
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Na-([(5R)-5-tert-butyl-2-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-2,5-dihydro-1H-pyrrol-3-yl]carbonyl)-L-phenylalaninamide
with anti-tumor activity; with anti-tumor activity
NPFREKKFFCAIL
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biotin-gamma6, substrate inhibition at high peptide concentration
P61A6
derived from an allenoate-derived compound library, shows efficiency of the enzyme inhibitor to inhibit tumor growth demonstrated using human pancreatic cancer xenograft; derived from an allenoate-derived compound library, shows efficiency of the enzyme inhibitor to inhibit tumor growth demonstrated using human pancreatic cancer xenograft
PD-083176
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noncompetitive to geranylgeranyl diphosphate, competitive to GST-CDC42, modest inhibitor
Phenylglyoxal
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80% loss of activity, inactivation of inhibition in the presence of geranylgeranyl diphosphate
tetrapeptide CVIL
superposition of the crystal structures of the CVIL-GGTase-I complex; superposition of the crystal structures of the CVIL-GGTase-I complex
Thr-Lys-Cys-Val-Ile-Leu
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potent competitor, 50% inhibition at 0.001 mM
Thr-Lys-Cys-Val-Ile-Met
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potent competitor, 50% inhibition at 0.008 mM
tipifarnib
the cdc43DELTA mutant is 4fold more susceptible to this farnesyltransferase inhibitor than the wild-type
umbelliprenine
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0.1 mM, 13.4% inhibition
[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetic acid benzyl ester
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IC50: above 0.01 mM
{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-acetic acid
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IC50: above 0.01 mM
{2-[3-(1H-imidazol-4-ylmethyl)-2,4-dioxo-3,4-dihydro-2H-quinazolin-1-yl]-acetylamino}-acetic acid methyl ester
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IC50: above 0.01 mM
(2S,5S)-5-tert-butyl-2-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-2,5-dihydro-1H-pyrrole-3-carboxylic acid
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IC50: 0.0005 mM using RhoA as a substrate, IC50: 0.0009 mM using Ki-Ras4B as a substrate
(2S,5S)-5-tert-butyl-2-(4-chlorophenyl)-1-[(2-methylphenyl)sulfonyl]-2,5-dihydro-1H-pyrrole-3-carboxylic acid
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1-phosphono-(E,E,E)-geranylgeraniol
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competitive to geranylgeranyl diphosphate, noncompetitive to GST-CDC42
1-phosphono-(E,E,E)-geranylgeraniol
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competitive to geranylgeranyl diphosphate, potent substrate inhibition to dansyl-Gly-Cys-Ile-Ile-Leu
GGTi-2147
specific GGTIbeta enzyme inhibitor; specific GGTIbeta enzyme inhibitor
GGTi-2147
specific GGTIbeta enzyme inhibitor; specific GGTIbeta enzyme inhibitor
GGTi-2147
a potent and selective inhibitor of GGT; potent and selective inhibitor of GGT
GGTi-2147
specific GGTIbeta enzyme inhibitor; specific GGTIbeta enzyme inhibitor
GGTI-298
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induces apoptosis and augments tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human lung cancer cells. GGTI-298 induces DR4 and DR5 expression and reduces c-FLIP levels. Enforced c-FLIP expression or DR5 knockdown attenuates apoptosis induced by GGTI-298 and TRAIL combination. DR4 knockdown sensitizes cancer cells to GGTI298/TRAIL-induced apoptosis. The combination of GGTI-298 and TRAIL is more effective than each single agent in decreasing the levels of IkappaBalpha and p-Akt
GGTI-298
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treatment of airway smooth muscle cells induces expression of p53-dependent proteins, p53 upregulated modulator of apoptosis Noxa, and damage-regulated autophagy modulator DRAM, this is inhibited by the p53 transcriptional activation inhibitor cyclic-pifithrin-alpha. Inhibition of autophagy with bafilomycin-A1 or short-hairpin RNA silencing of Atg7 substantially augments GGTI-298-induced apoptosis
GGTI-DU40
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1-40 microM dissolved in dimethyl sulfoxide, affects actin cytoskeletal integrity, cell adhesion, cell-cell junctions, myosin II phosphorylation, and membrane localization of GTP-binding proteins in trabecular meshwork cells is tested using immunofluorescence detection and immunoblotting analysis and the effect on aqueous humor outflow
GGTI-DU40
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5-40 microM dissolved in dimethyl sulfoxide influence cell morphology in a dose and time dependent manner, affects actin cytoskeletal integrity, cell adhesion, cell-cell junctions, myosin II phosphorylation, and membrane localization of GTP-binding proteins in trabecular meshwork cells is tested using immunofluorescence detection and immunoblotting analysis and the effect on aqueous humor outflow (25 and 40 microM)
GGTI-DU40
16.3% inhibition at 50 nM
L-269289
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inhibitor L-269289 and echinocandins act in a synergistic manner for the treatment of Candida parapilosis
L-269289
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inhibitor L-269289 and echinocandins act in a synergistic manner for the treatment of Candida tropicalis
L-269289
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inhibitor L-269289 is active on its own to kill Candida glabrata, and its fungicidal activity is enhanced when combined with caspofungin
additional information
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not inhibited by valencic acid, 4'-geranyloxybenzoic acid, 4-isopentenyloxy-3-methoxy benzoic acid, and 4-geranyloxy-3-methoxy benzoic acid
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additional information
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not inhibited by 3,4,5-tris(3-amino-4-phenyl-1-butoxy)benzoic acid methyl ester trifluoroacetate and mono(3,3',3''-(5-(methoxycarbonyl)benzene-1,2,3-triyl)tris(oxy)tripropan-1-aminium) mono(2,2,2-trifluoroacetate)
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additional information
most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors. Inhibition mechanisms for FTase, EC 2.5.1.58, and GGTase-I are different. Molecular modeling studies of GGTase-I and protein-inhibitor interactions, overview; most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors. Inhibition mechanisms for FTase, EC 2.5.1.58, and GGTase-I are different. Molecular modeling studies of GGTase-I and protein-inhibitor interactions, overview
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additional information
most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors. Inhibition mechanisms for FTase, EC 2.5.1.58, and GGTase-I are different. Molecular modeling studies of GGTase-I and protein-inhibitor interactions, overview; most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors. Inhibition mechanisms for FTase, EC 2.5.1.58, and GGTase-I are different. Molecular modeling studies of GGTase-I and protein-inhibitor interactions, overview
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additional information
nanoformulation of geranylgeranyltransferase-I inhibitors for cancer therapy, liposomal encapsulation and pH-dependent delivery to cancer cells, scheme of synthesis of pH-responsive liposome and the proposed intracellular drug release pathway, method, overview. Liposomal GGTI inhibits protein geranylgeranylation inside the cell and this effect is dependent on the low pH of lysosomes; nanoformulation of geranylgeranyltransferase-I inhibitors for cancer therapy, liposomal encapsulation and pH-dependent delivery to cancer cells, scheme of synthesis of pH-responsive liposome and the proposed intracellular drug release pathway, method, overview. Liposomal GGTI inhibits protein geranylgeranylation inside the cell and this effect is dependent on the low pH of lysosomes
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additional information
nanoformulation of geranylgeranyltransferase-I inhibitors for cancer therapy, liposomal encapsulation and pH-dependent delivery to cancer cells, scheme of synthesis of pH-responsive liposome and the proposed intracellular drug release pathway, method, overview. Liposomal GGTI inhibits protein geranylgeranylation inside the cell and this effect is dependent on the low pH of lysosomes; nanoformulation of geranylgeranyltransferase-I inhibitors for cancer therapy, liposomal encapsulation and pH-dependent delivery to cancer cells, scheme of synthesis of pH-responsive liposome and the proposed intracellular drug release pathway, method, overview. Liposomal GGTI inhibits protein geranylgeranylation inside the cell and this effect is dependent on the low pH of lysosomes
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additional information
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nanoformulation of geranylgeranyltransferase-I inhibitors for cancer therapy, liposomal encapsulation and pH-dependent delivery to cancer cells, scheme of synthesis of pH-responsive liposome and the proposed intracellular drug release pathway, method, overview. Liposomal GGTI inhibits protein geranylgeranylation inside the cell and this effect is dependent on the low pH of lysosomes; nanoformulation of geranylgeranyltransferase-I inhibitors for cancer therapy, liposomal encapsulation and pH-dependent delivery to cancer cells, scheme of synthesis of pH-responsive liposome and the proposed intracellular drug release pathway, method, overview. Liposomal GGTI inhibits protein geranylgeranylation inside the cell and this effect is dependent on the low pH of lysosomes
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additional information
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inhibitors pose a potential treatment for inflammation, multiple sclerosis, atherosclerosis, and other diseases, 47 potential inhibitors with a predicted IC50 greater than 5.50 microM are identified by the use of quantitative structure-activity relationship models and in vitro tests with 7 of them
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additional information
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TKSer-Val-Ile-Leu inactive as competitor
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additional information
most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors; most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors
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additional information
most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors; most GGT inhibitors are CAAX-competitive inhibitors, except for a few GGPP-competitive inhibitors
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additional information
the mammalian PGGT-I inhibitors GGTI-297 and FTI-276 have little effect on Trypanosoma cruzi PGGT-I activity
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additional information
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the mammalian PGGT-I inhibitors GGTI-297 and FTI-276 have little effect on Trypanosoma cruzi PGGT-I activity
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