Home
Drugs
Targets
Pathways
Ontologies
Cyp450s
Adv.search
Help/FAQ

Drug-Target Interaction

Drug

show drug details
PubChem ID:16741
Structure:
Synonyms:
(2-Isothiocyanato-ethyl)-benzene
(2-isothiocyanatoethyl)benzene
.beta.-Phenethyl isothiocyanate
.beta.-Phenylethyl isothiocyanate
1-(2-isothiocyanatoethyl)benzene
2-isothiocyanatoethylbenzene
2-phenethyl isothiocyanate
2-phenyl ethyl isothiocyanate
2-Phenylethyl isothiocyanate
2-phenylethylisothiocyanate
2257-09-2
253731_ALDRICH
4-12-00-02476 (Beilstein Handbook Reference)
A-Phenethyl isothiocyanate
AB1006056
AC-12769
AC1L28L3
AKOS000119469
b-phenylethyl isothiocyanate
BB_SC-1856
Benzene, (2-isothiocyanatoethyl)-
beta-Phenethyl isothiocyanate
beta-phenethylisothiocyanate
beta-Phenylethyl isothiocyanate
BRN 2084162
C058305
C9H9NS
CCRIS 3146
CHEBI:351346
CHEMBL151649
EINECS 218-855-5
HMS1783C17
I01-3453
I01-8790
Isothiocyanic Acid 2-Phenylethyl Ester
Isothiocyanic acid beta-phenylethyl ester
Isothiocyanic acid, phenethyl ester
IZJDOKYDEWTZSO-UHFFFAOYSA-
LS-7646
MolPort-000-146-876
NCGC00248526-01
NCI60_041942
NSC 87868
NSC87868
P0986
PEITC
PEITC compound
Phenethyl isothiocyanate
Phenethyl mustard oil
Phenylaethylsenfoel
Phenylaethylsenfoel [German]
Phenylethyl isothiocyanate
Phenylethyl mustard oil
STK397325
W401404_ALDRICH
WLN: SCN2R
ZERO/008133
ZINC02022074

Target

show target details
Uniprot ID:ICE_DROME
Synonyms:
Caspase
drICE
EC-Numbers:3.4.22.-
Organism:Drosophila melanogaster
Fruit fly
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----
----
----

References:

14729592
The chemopreventive agent phenethyl isothiocyanate sensitizes cells to Fas-mediated apoptosis.. Juliet M Pullar; Susan J Thomson; Monica J King; Christopher I Turnbull; Robyn G Midwinter; Mark B Hampton (2004) Carcinogenesis display abstract
The chemopreventive properties of the isothiocyanates have been attributed to their ability to inhibit phase I enzymes that activate procarcinogens, induce phase II protective enzymes and trigger apoptosis in transformed cells. In this study we provide evidence for a new mechanism of chemoprevention, wherein sublethal doses of phenethyl isothiocyanate (PEITC) sensitize cells to Fas-mediated apoptosis. The phenomenon was observed in the Fas-resistant T24 bladder carcinoma cell line and in Jurkat T cells overexpressing the anti-apoptotic protein Bcl-2. Caspase-3-like activity was increased up to 20-fold of that observed with either PEITC or anti-Fas antibody alone. While PEITC activated ERK, JNK and p38, inhibitors of these MAP kinases did not block apoptosis. PEITC transiently depleted cellular glutathione, providing a putative mechanism for sensitizing the cells to apoptosis. However, lowering glutathione with buthionine sulfoximine did not mimic the effect of PEITC. Instead, we propose that PEITC promotes apoptosis by directly modifying intracellular thiol proteins. The ability of PEITC to sensitize cells to receptor-mediated apoptosis provides an additional mechanism to explain its chemopreventive properties.
16624391
Phenethyl isothiocyanate (PEITC) inhibits growth of ovarian cancer cells by inducing apoptosis: role of caspase and MAPK activation.. K S Satyan; Narasimha Swamy; Don S Dizon; Rakesh Singh; Cornelius O Granai; Laurent Brard (2006) Gynecologic oncology display abstract
OBJECTIVE: Epithelial ovarian cancer has the highest mortality rate among gynecologic cancers. Chemotherapy is an essential component of its treatment. While isothiocyanates are known to possess chemopreventive effects against various cancers, yet little is known about their chemotherapeutic potential in ovarian cancer (OC). In the present study, we examined the antiproliferative and apoptotic effect of phenethyl isothiocyanate (PEITC), a naturally occurring isothiocyanate on OVCAR-3 cells. METHODS: Cytotoxic activity of PEITC on OVCAR-3 cells was determined using cell proliferation, apoptosis (DNA fragmentation and TUNEL assay) and caspase-activation studies. The role of PARP-1, Bax, and Bcl-2 in apoptosis was analyzed by Western blotting. Activation of JNK1/2, p38, Akt, ERK1/2, and c-Myc was examined by immunoblotting. Specific inhibitors of caspases, JNK1/2, p38, and MEK were used to corroborate these data. RESULTS: PEITC was cytotoxic to OVCAR-3 cells, and inhibited proliferation in a dose-dependent fashion (IC(50) = 23.2 microM). PEITC induced apoptosis by activating caspase-3 and -9, without capsase-8 activation. Anti-apoptotic Bcl-2 levels were suppressed while pro-apoptotic Bax levels were enhanced. PEITC suppressed activation of Akt, ERK1/2, and the expression of transcription factor c-Myc, while simultaneously activating pro-apoptotic p38 and JNK1/2. Specific inhibitors of caspase-3 and -9, JNK1/2, and p38 reversed the cytotoxic effect of PEITC. CONCLUSIONS: These findings demonstrate that PEITC exhibits cytotoxicity towards OVCAR-3 cells and induces apoptosis via caspase-9 and -3 pathways. PEITC inhibits Akt, ERK1/2 survival signaling, and c-Myc while simultaneously activating pro-apoptotic p38 and JNK1/2. Systematic preclinical and clinical trials with PEITC in ovarian cancer are indicated.
9458080
Chemopreventive isothiocyanates induce apoptosis and caspase-3-like protease activity.. R Yu; S Mandlekar; K J Harvey; D S Ucker; A N Kong (1998) Cancer research display abstract
Isothiocyanates exert strong anticarcinogenic effects in a number of animal models of cancer, presumably by modulation of xenobiotic-metabolizing enzymes, such as by inhibition of cytochrome P-450 and/or by induction of phase II detoxifying enzymes. Here, we report that phenethyl isothiocyanate and other structurally related isothiocyanates, phenylmethyl isothiocyanate, phenylbutyl isothiocyanate, and phenylhexyl isothiocyanate, but not phenyl isothiocyanate induced apoptosis in HeLa cells in a time- and dose-dependent manner. Treatment with apoptosis-inducing concentrations of isothiocyanates also caused rapid and transient induction of caspase-3/CPP32-like activity. Furthermore, these isothiocyanates, except phenyl isothiocyanate, stimulated proteolytic cleavage of poly(ADP-ribose) polymerase, which followed the appearance of caspase activity and preceded DNA fragmentation. Pretreatment with a potent caspase-3 inhibitor acetyl-Asp-Glu-Val-Asp-aldehyde inhibited isothiocyanate-induced caspase-3-like activity and apoptosis. These results suggest that isothiocyanates may induce apoptosis through a caspase-3-dependent mechanism. The induction of apoptosis by isothiocyanates may provide a distinct mechanism for their chemopreventive functions.