Delving into the Latest Updates on Norethisterone/Ethinyl estradiol with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Norethisterone/Ethinylestradiol

+ [5]

Target

ER x PR

Action

agonists

Mechanism

ERs agonists(Estrogen receptors agonists), PR agonists(Progesterone receptor agonists)

Therapeutic Areas

Nervous System DiseasesOther Diseases

Active Indication

DysmenorrheaContraception

Inactive Indication

EndometriosisPrimary dysmenorrhea

Originator Organization

Daiichi Seiyaku Co., Ltd.Syntex Corp.

Active Organization

Nobelpharma Co., Ltd.

Kaken Pharmaceutical Co., Ltd.

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date

Japan (16 Jun 1999),

Contraception

Regulation-

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Structure/Sequence

Molecular FormulaC40H50O4

InChIKeyNAPPWIFDUAHTRY-XYDRQXHOSA-N

CAS Registry37270-71-6

The purpose of this study is to assess the pharmacokinetic profiles of norethisterone and ethinyl estradiol after single oral administration of NPC-01 in healthy female volunteers.
Pharmacokinetics of norethisterone and ethinyl estradiol will be evaluated on the basis of AUC, Cmax, tmax, t1/2, MRT, kel and AUC∞.

Start Date01 Nov 2010

Sponsor / Collaborator

Nobelpharma Co., Ltd.

100 Clinical Results associated with Norethisterone/Ethinyl estradiol

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100 Translational Medicine associated with Norethisterone/Ethinyl estradiol

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100 Patents (Medical) associated with Norethisterone/Ethinyl estradiol

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199

Literatures (Medical) associated with Norethisterone/Ethinyl estradiol

01 Mar 2024·Bioorganic & Medicinal Chemistry

Target fishing reveals PfPYK-1 and PfRab6 as potential targets of an antiplasmodial 4-anilino-2-trichloromethylquinazoline hit compound

Article

Author: Vanelle, P ; Dumètre, A ; Ruchaud, S ; Primas, N ; Gaillard, F ; Rault, S ; Rathelot, P ; Renault, J ; Merckx, A ; Hutter, S ; Kieffer, C ; Verhaeghe, P ; Reininger, L ; Hervé, L ; Laget, M ; Azas, N ; Castera-Ducros, C ; Bach, S ; Doerig, C ; Amrane, D

We present investigations about the mechanism of action of a previously reported 4-anilino-2-trichloromethylquinazoline antiplasmodial hit-compound (Hit A), which did not share a common mechanism of action with established commercial antimalarials and presented a stage-specific effect on the erythrocytic cycle of P. falciparum at 8 < t < 16 h. The target of Hit A was searched by immobilising the molecule on a solid support via a linker and performing affinity chromatography on a plasmodial lysate. Several anchoring positions of the linker (6,7 and 3') and PEG-type linkers were assessed, to obtain a linked-hit molecule displaying in vitro antiplasmodial activity similar to that of unmodified Hit A. This allowed us to identify the PfPYK-1 kinase and the PfRab6 GTP-ase as potential targets of Hit A.

01 Jun 2018·Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

[NSD3 suppresses LPS-triggered TNF-α production via promoting the dimethylation of histone H3K36 in macrophages].

Article

Author: Liu, Zhaolong ; Sun, Yanxiang ; Yang, Le ; Cheng, Qijiang

Objective To investigate the role of nuclear receptor-binding SET domain protein 3 (NSD3) in lipopolysaccharide (LPS)-triggered tumor necrosis factor α (TNF-α) production in macrophages and the underlying epigenetic mechanism. Methods The experiment used murine peritoneal macrophages and RAW264.7 cells as cell models. The mRNA and protein level of NSD3 were detected by real-time quantitative PCR and Western blot analysis in mouse peritoneal macrophages stimulated with LPS (100 ng/mL). ELISA was used to detect the production of TNF-α in NSD3-overexpressing RAW264.7 cells or NSD3-silencing peritoneal macrophages. Western blot analysis was performed to test the activation of LPS-triggered NF-κBp65 in NSD3-silencing macrophages. Luciferase assay was used to assess NF-κBp65-mediated transcriptional activation of TNF-α gene. ChIP assay was used to detect the recruitment of H3K36 methylation to TNF-α gene promoter. Results LPS inhibited the expression of NSD3 in the macrophages. Over-expression of NSD3 suppressed LPS-triggered TNF-α production, and silencing NSD3 promoted LPS-triggered TNF-α production. However, NSD3 had no effect on the activation of LPS-triggered NF-κBp65. NSD3 enhanced NF-κBp65-mediated transcriptional activation of TNF-α gene. NSD3 enhanced the dimethylation of H3K36 of TNF-α gene promoter. Conclusion NSD3 can promote the dimethylation of H3K36 of TNF-α gene promoter and suppress TNF-α transcription and production.

01 Dec 2016·Fertility and SterilityQ2 · MEDICINE

Evaluation of an ultra-low-dose oral contraceptive for dysmenorrhea: a placebo-controlled, double-blind, randomized trial

Q2 · MEDICINE

Article

Author: Momoeda, Mikio ; Harada, Tasuku

OBJECTIVETo evaluate the efficacy and safety of an ultra-low-dose oral contraceptive (NPC-01; 0.02 mg ethinyl estradiol and 1 mg norethisterone) in subjects with dysmenorrhea.DESIGNPlacebo-controlled, double-blind, randomized trial.SETTINGClinical trial sites.PATIENT(S)Two hundred fifteen subjects with dysmenorrhea.INTERVENTION(S)Subjects were randomly assigned to receive NPC-01, placebo, or IKH-01 (0.035 mg ethinyl estradiol and 1 mg norethisterone) for four cycles.MAIN OUTCOME MEASURE(S)Total dysmenorrhea score (verbal rating scale) assessing pain on the basis of limited ability to work and need for analgesics.RESULT(S)The reductions of total dysmenorrhea score and visual analog scale score after the treatment were significantly higher in the NPC-01 group than in the placebo group. Furthermore, the efficacy of NPC-01 was comparable to that of IKH-01. The overall incidence of side effects was significantly higher in the NPC-01 group than in the placebo group. All side effects that occurred in the NPC-01 group were previously reported in patients receiving IKH-01. No serious side effects occurred.CONCLUSION(S)The ultra-low-dose contraceptive NPC-01 relieved dysmenorrhea as effectively as IKH-01. Thus, NPC-01 could represent a new option for long-term treatment of dysmenorrhea.CLINICAL TRIAL IDENTIFICATION NUMBERNCT01129102.

100 Deals associated with Norethisterone/Ethinyl estradiol

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R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Dysmenorrhea	Japan	Nobelpharma Co., Ltd.	16 Apr 2008
Contraception	Japan	Kaken Pharmaceutical Co., Ltd.	16 Jun 1999

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Primary dysmenorrhea	Discovery	-	Nobelpharma Co., Ltd.	01 Sep 2008
Endometriosis	Discovery	-	Nobelpharma Co., Ltd.	01 Dec 2004

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01246791 (CTgov)	Phase 3	-	12	NPC-01	ujqdsvrsfn(vyedqildfn) = lhywekfpri pprhyqiqwp (iytrhhzsdi, ztfzykpbrm - jqyqvnjqpu) View more	-	17 Jun 2014
NCT01129102 (CTgov)	Phase 3	Dysmenorrhea	215	NPC-01 (NPC-01)	zbquvsdyfk(hrvnhpjzrk) = ftawkibuee ystgnmbydx (knaffycfoa, ptbrjdmjce - ussgjlwhti) View more	-	17 Jun 2014
				Placebo (Placebo)	zbquvsdyfk(hrvnhpjzrk) = krgqbsgnsx ystgnmbydx (knaffycfoa, hmekaakdlq - qxvdkjccwt) View more
NCT01253824 (CTgov)	Phase 3	-	14	NPC-01 (NPC-01)	ldecdjwfeq(vkhfpkmtej) = drajplmerj pkwonihviq (cswgwzuxej, xcptlvmtol - fqjpbjzjnf) View more	-	17 Jun 2014
				IKH-01 (IKH-01)	ldecdjwfeq(vkhfpkmtej) = bnudcyrcpn pkwonihviq (cswgwzuxej, bgceokiatr - sdmwahuwba) View more
NCT00902746 (CTgov)	Phase 3	Endometriosis \| Dysmenorrhea	149	NPC-01	ggtvamjrot(uyqhyzesvg) = yqmkgbbstj uselilldvc (xmtceglkoe, lxiblkahmd - zfjhqgrqaw) View more	-	13 Jun 2014
NCT00746096 (CTgov)	Phase 3	Primary dysmenorrhea	115	IKH-01 (IKH-01)	pdvxpbfwqr(srsyvqbtnk) = vjlssuziwr eyrqspynti (xceuvwesbc, siqfjatlvs - botisliefj) View more	-	13 Jun 2014
				Placebo (Placebo)	pdvxpbfwqr(srsyvqbtnk) = bhyuopbkph eyrqspynti (xceuvwesbc, jbjdndtfqk - pglmlkddqf) View more