DHEA

"目录号: HY-14650

Others-

DHEA 是雄激素重要来源,是一种有效的抗细胞凋亡因子。

Androgen Receptor

相关产品

Enzalutamide-Dihydrotestosterone-Testosterone-ARN-509-Bicalutamide-ODM-201-ASC-J9-MK-0773-Spironolactone-AZD3514-Flutamide-LGD-4033-3,3'-Diindolylmethane-GLPG0492-Danazol-

生物活性

Description

DHEA is an important source ofandrogens, and is an effective antiapoptotic factor.

IC50& Target

Androgen receptor[1]

In Vitro

DHEA is an effective antiapoptotic factor, reversing the serum deprivation-induced apoptosis in prostate cancer cells (DU145 and LNCaP cell lines) as well as in colon cancer cells (Caco2 cell line). DHEA significantly reduces serum deprivation-induced apoptosis in all 3 cancer cell types, quantitated with the APOPercentage assay (apoptosis is reduced from 0.587±0.053 to 0.142±0.0016 or 0.059±0.002 after treatment for 12 hours with DHEA or NGF, respectively; n=3, P<0.01), and by flow cytometry analysis (FACS) for DU145 cells. The antiapoptotic effect of DHEA is dose dependent with an EC50 at nanomolar concentrations (EC50: 11.2±3.6 nM and 12.4±2.2 nM in DU145 and Caco2 cells, respectively)[1]. DHEA is the principal sex steroid precursor in humans and can be converted directly to androgens. DHEA (≥1 μM) causes a dose-dependent inhibition of Chub-S7 proliferation, as assessed by thymidine incorporation assays. DHEA treatment inhibits expression of the key glucocorticoid-regulating genesH6PDH(≥100 nM) andHSD11B1(≥1 μM) in differentiating preadipocytes in a dose-dependent manner. In keeping with this finding, DHEA treatment (≥1 μM) results in a marked reduction in 11β-HSD1 oxoreductase activity (≥1 μM) and a concurrent increase in dehydrogenase activity at the highest DHEA dose used (25 μM DHEA) in differentiated adipocytes[2].

In Vivo

DHEA in the diet (0.45 % w/w) of male B6 mice (groups of five mice) treated for 8 weeks led to significant decreases in body temperature compared with mice fed the control AIN-76A diet. A similar comparison indicated that control and pair-fed mice are also significantly different. Animals fed DHEA have significantly lower temperatures than mice fed the control diet 26/29 times tested; mice pair fed to those on the DHEA diet are less affected, with 8/29 values significantly lower than in mice fed AIN-76Aad libitum. The temperatures of mice fed DHEA or pair fed to DHEA are significantly different 21/29 times tested. Body weights are significantly greater in mice fed the control diet than in mice fed DHEA or pair fed to DHEA. Food intake (grams per day) from cages are averaged for each week (n=7), except for Week 9 (n=3). The amount of food intake is significantly decreased in mice fed DHEA. By design, mice pair fed to DHEA ate about the same amount. Thus, it appears that DHEA reduces body temperature by food restriction and by a separate mechanism[3].

Clinical Trial

NCT02357472

ShangHai Ji Ai Genetics & IVF Institute

Infertility

December 2014

Phase 4

NCT02150330

Taipei Veterans General Hospital, Taiwan-National YangMing University

Dehydroepiandrosterone-DHEAS-Gene Expression of Cumulus Cells.-Ovarian Hyper-stimulation Protocol.-Artificial Reproduction Technology.

January 2013

Phase 3

NCT00575341

University Hospital Tuebingen

Adrenal Insufficiency

October 2003

Phase 3

NCT00289926

Monash University

Quality of Life-Menopausal Syndrome-Libido Disorder

February 2006

Phase 3

NCT00900900

Jed E. Rose-Duke University

Substance Withdrawal Syndrome

July 2009

Phase 2

NCT00650754

Center for Human Reproduction

Primary Ovarian Insufficiency-Unexplained Infertility

March 2008

Phase 2-Phase 3

NCT02432248

The Affiliated Hospital of Inner Mongolia Medical University-First Affiliated Hospital, Sun Yat-Sen University-Renmin Hospital of Wuhan University

Subfertility

February 2015

NCT00948857

David H. Barad-Center for Human Reproduction

Premature Ovarian Failure

June 2009

Phase 2-Phase 3

NCT01861847

Humanetics Corporation

PTSD

February 2013

Phase 2

NCT00419913

Center for Human Reproduction-Foundation for Reproductive Medicine

Infertility-Decreased Ovarian Reserve

January 2007

Phase 2-Phase 3

NCT00916396

Tel-Aviv Sourasky Medical Center

Hypoactive Sexual Desire Disorder

June 2005

NCT01535872

KK Women's and Children's Hospital

Infertility-Poor Responder to IVF Treatment

February 2012

Phase 3

NCT00248989

CHU de Quebec-Universite Laval

Skin Aging-Quality of Life

November 1, 2004

Phase 3

NCT01129830

Virginia Center for Reproductive Medicine

Infertility

January 2010

Early Phase 1

NCT00391924

UMC Utrecht-University Medical Center Groningen-Dutch Arthritis Association

Lupus Erythematosus, Systemic-Sjogren's Syndrome

May 2000

Phase 2

NCT01572025

University of Nottingham

Infertility-Ovarian Aging-Diminished Ovarian Reserve (DOR)-Predicted Poor-responders

May 2012

Phase 3

NCT00167609

University of Versailles-Association Française contre les Myopathies (AFM), Paris-Assistance Publique - Hôpitaux de Paris

Myotonic Dystrophy

November 2004

Phase 2-Phase 3

NCT00001598

National Institute of Dental and Craniofacial Research (NIDCR)-National Institutes of Health Clinical Center (CC)

Lacrimal Apparatus Disease-Salivary Gland Disease-Sjogren's Syndrome-Xerostomia

May 1997

Phase 2

NCT00189124

University of Michigan-Arthritis Foundation

Systemic Lupus Erythematosus

September 2003

Phase 2-Phase 3

NCT01145144

Meir Medical Center

Ovarian Stimulation

January 2008

NCT00543166

Helsinki University-Göteborg University-Uppsala University

Sjogren's Syndrome

February 2003

Phase 4

NCT00607646

University of Maryland-National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Type 1 Diabetes

October 2010

Early Phase 1

NCT00442403

Université Victor Segalen Bordeaux 2

Malaria

April 2002

Phase 3

NCT00471900

University of Aarhus

Adrenal Insufficiency

October 2001

NCT00001487

National Institute of Mental Health (NIMH)-National Institutes of Health Clinical Center (CC)

Depressive Disorder-Mood Disorder

June 1995

Phase 2

NCT00566384

Bayer

Libido

November 2007

Phase 2

NCT00004795

National Center for Research Resources (NCRR)-Northwestern University-Office of Rare Diseases (ORD)

Systemic Lupus Erythematosus

August 1994

Phase 2-Phase 3

NCT00004665

National Center for Research Resources (NCRR)-Northwestern University-Office of Rare Diseases (ORD)

Systemic Lupus Erythematosus

June 1995

Phase 2

NCT00004662

National Center for Research Resources (NCRR)-Northwestern University-Office of Rare Diseases (ORD)

Systemic Lupus Erythematosus

March 1996

Phase 3

NCT00004313

National Center for Research Resources (NCRR)-University of California, Los Angeles-Office of Rare Diseases (ORD)

Addison's Disease

August 1995

Phase 3

NCT02794948

Guangzhou University of Traditional Chinese Medicine

Primary Ovarian Insufficiency

April 2016

Early Phase 1

NCT01753037

Mayo Clinic

Hyperandrogenism

December 2006

NCT00310791

Boston Children’s Hospital-United States Department of Defense-Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)

Anorexia Nervosa

April 2004

Phase 2-Phase 3

NCT00106314

Inflabloc Pharmaceuticals

Crohn's Disease

January 2005

Phase 2

NCT00673309

The University of Texas Medical Branch, Galveston-National Institutes of Health (NIH)

Burns

July 2002

Phase 2-Phase 3

NCT02013544

EndoCeutics Inc.

Vaginal Atrophy

February 2014

Phase 3

NCT00082511

Genelabs Technologies

Systemic Lupus Erythematosus

July 2003

Phase 3

NCT01376349

Alliance for Clinical Trials in Oncology-National Cancer Institute (NCI)-Mayo Clinic

Breast Cancer-Gynecologic Cancer

July 2011

Phase 3

NCT00053560

Genelabs Technologies

Lupus

December 2002

Phase 3

NCT00006219

Mayo Clinic-National Cancer Institute (NCI)

Multiple Myeloma and Plasma Cell Neoplasm

August 2000

Phase 2

NCT01343771

Boston Children’s Hospital

Anorexia Nervosa (AN)

June 2011

Phase 3

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References

[1].Anagnostopoulou V, et al. Differential effects of dehydroepiandrosterone and testosterone in prostate and colon cancer cell apoptosis: the role of nerve growth factor (NGF) receptors. Endocrinology. 2013 Jul;154(7):2446-56.

[2].McNelis JC, et al. Dehydroepiandrosterone exerts anti-glucocorticoid action on human preadipocyte proliferation, differentiation and glucose uptake. Am J Physiol Endocrinol Metab. 2013 Nov 1;305(9):E1134-44.

[3].Catalina F, et al. Decrease of core body temperature in mice by dehydroepiandrosterone. Exp Biol Med (Maywood). 2002 Jun;227(6):382-8.

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