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Drug-Target Interaction

Drug

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PubChem ID:4536
Structure:
Synonyms:
14-ethynyl-14-hydroxy-15-methyltetracyclo[8.7.0.0<2,7>.0<11,15>]heptadec-6
17-Ethynyl-17-hydroxyestr-4-en-3-one
17-Hydroxy-19-nor-17.alpha.-pregn-4-en-20-yn-3-one
17.alpha.-Ethinyl-17.beta.-hydroxy-.delta.(sup:4)-estren-3-one
17.alpha.-Ethinyl-19-nortestosterone
17.alpha.-Ethinylestra-4-en-17.beta.-ol-3-one
17.alpha.-Ethynyl-17-hydroxy-4-estren-3-one
17.alpha.-Ethynyl-17.beta.-hydroxy-19-norandrost-4-en-3-one
17.alpha.-Ethynyl-17.beta.-hydroxyestr-4-en-3-one
17.alpha.-Ethynyl-19-nor-4-androsten-17.beta.-ol-3-one
17.alpha.-Ethynyl-19-norandrost-4-en-17.beta.-ol-3-one
17.alpha.-Ethynyl-19-nortestosterone
17.alpha.-Ethynyl-4-estren-17-ol-3-one
17.beta.-Hydroxy-19-norpregn-4-en-20-yn-3-one
17alpha-Ethynyl-17 beta-hydroxy-19-nor-4-androsten-3-one
19-nor-17.alpha.-Ethynyl-17.beta.-hydroxy-4-androsten-3-one
19-nor-17.alpha.-Ethynylandrosten-17.beta.-ol-3-one
19-Nor-17.alpha.-ethynyltestosterone
19-Nor-17.alpha.-pregn-4-en-20-yn-3-one, 17-hydroxy-
19-Norethisterone
19-Norpregn-4-en-20-yn-3-one, 17-hydroxy-, (17.alpha.)-
19-Nortestosterone, 17-ethynyl-
68-22-4
A3564/0151191
AC1L1IDS
AC1Q6OG5
Anhydrohydroxynorprogesterone
Anovule
AR-1C1071
component of Brevicon
component of Modicon
component of Neocon
component of Noriday
component of Norinyl
component of Ortho-Novum
component of Ovcon
Conludaf
Conludag
Estr-4-en-3-one, 17.alpha.-ethynyl-17-hydroxy-
Ethinylnortestosterone
Ethynylnortestosterone
Gestest
I06-0104
Micronett
Micronor
Micronovum
Mini-Pe
Minovlar
MolPort-002-728-977
Nor-Q.D.
Noralutin
Noresthisterone
Norethindrone
Norethisteron
Norethisterone
Norethyndron
Norethynodrone
Norfor
Norgestin
Noriday
Norlutate
Norluten
Norlutin
Norluton
Norpregneninlone
Norpregneninolone
NSC-9564
NSC9564
Oprea1_606355
Primolut N
Proluteasi
SC 4640
ST094767
STK730956
TULIP017664
Utovlar
WLN: L E5 B666 OV MUTJ E FQ F1UU1 -A&F
Side-Effects:
Side-EffectFrequency
spontaneous abortion0
pulmonary embolism0
seizures0
venereal disease0
tuberculosis0
urticaria0
weight gain0
cerebral thrombosis0
emotional lability0
deep vein thrombosis0
migraine0
menstrual irregularity0
breast tenderness0
blindness0
lump0
acne0
pruritus0
pain0
ovarian cyst0
dizziness0
edema0
embolism0
rash0
headache0
hemorrhage0
hirsutism0
breast enlargement0
jaundice0
melasma0
menstrual flow0
metrorrhagia0
nausea0
tumor0
optic neuritis0
insomnia0

Target

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Uniprot ID:CP3A4_HUMAN
Synonyms:
Albendazole monooxygenase
Albendazole sulfoxidase
CYPIIIA3
CYPIIIA4
Cytochrome P450 3A3
Cytochrome P450 3A4
HLp
NF-25
Nifedipine oxidase
P450-PCN1
Quinine 3-monooxygenase
Taurochenodeoxycholate 6-alpha-hydroxylase
EC-Numbers:1.14.13.32
1.14.13.67
1.14.13.97
Organism:Homo sapiens
Human
PDB IDs:1TQN 1W0E 1W0F 1W0G 2J0D 2V0M
Structure:
2V0M

Binding Affinities:

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

References:

14663455
18356043
Identification of the human cytochrome P450 enzymes involved in the in vitro biotransformation of lynestrenol and norethindrone.. Tuomas Korhonen; Miia Turpeinen; Ari Tolonen; Kari Laine; Olavi Pelkonen (2008) The Journal of steroid biochemistry and molecular biology display abstract
This study examined the cytochrome P450 (CYP) enzyme selectivity of in vitro bioactivation of lynestrenol to norethindrone and the further metabolism of norethindrone. Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM). Fluconazole modestly inhibited both lynestrenol bioactivation and norethindrone biotransformation. Lynestrenol bioactivation was mainly catalysed by recombinant human CYP2C9, CYP2C19 and CYP3A4; rCYP3A4 was responsible for the hydroxylation of norethindrone. A significant correlation was observed between norethindrone formation and tolbutamide hydroxylation, a CYP2C9-selective activity (r=0.63; p=0.01). Norethindrone hydroxylation correlated significantly with model reactions of CYP2C19 and CYP3A4. The greatest immunoinhibition of lynestrenol bioactivation was seen in incubations with CYP2C-Ab. The CYP3A4-Ab reduced norethindrone hydroxylation by 96%. Both lynestrenol and norethindrone were weak inhibitors of CYP2C9 (IC(50) of 32 microM and 46 microM for tolbutamide hydroxylation, respectively). In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone.