Non-steroidal glucocorticoid receptor antagonists: The race to replace RU-486 for anti-glucocorticoid therapy

Michael L. Mohler, Yali He, Zhongzhi Wu, Seoung Soo Hong, Duane Miller

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

The endogenous glucocorticoid, cortisol, elevates blood glucose and suppresses the immune system. Glucocorticoid (GC) levels rapidly increase in response to physiologic and mental stress, thereby allowing stress adaptation. Unfortunately, the GC response can be excessive, especially under stressful conditions for the organism. The resulting hypercortisolemia is associated with a cluster of symptoms called Cushing's syndrome, a serious and potentially fatal illness involving hyperglycemia, hypertension, osteoporosis, muscle atrophy and fat maldistribution, as well as psychoses and immunosuppresion. Several disease states, such as diabetes and Cushing's, would benefit from blocking the actions of endogenous cortisol. The only glucocorticoid receptor (GR) antagonist available in the clinic is the steroid mifepristone (RU-486), whose primary potency is antigestagenic, making its utility as a GR antagonist limited. This manuscript reviews the current patent literature on selective non-steroidal GR antagonists.

Original languageEnglish (US)
Pages (from-to)59-81
Number of pages23
JournalExpert Opinion on Therapeutic Patents
Volume17
Issue number1
DOIs
StatePublished - Jan 1 2007

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Mifepristone
Glucocorticoid Receptors
Glucocorticoids
Hydrocortisone
Literature
Patents
Muscular Atrophy
Cushing Syndrome
Hyperglycemia
Psychotic Disorders
Osteoporosis
Blood Glucose
Immune System
Therapeutics
Fats
Steroids
Hypertension

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Drug Discovery

Cite this

Non-steroidal glucocorticoid receptor antagonists : The race to replace RU-486 for anti-glucocorticoid therapy. / Mohler, Michael L.; He, Yali; Wu, Zhongzhi; Hong, Seoung Soo; Miller, Duane.

In: Expert Opinion on Therapeutic Patents, Vol. 17, No. 1, 01.01.2007, p. 59-81.

Research output: Contribution to journalReview article

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