A Randomized Double-blind Placebo-controlled Trial Comparing Letrozole Versus Mifepristone As Pre-treatment Before Medical Management of First Trimester Silent Miscarriage Using Misoprostol

Management of first trimester silent miscarriage can be by expectant, medical or surgical management. Surgical management by suction evacuation is associated with surgical risks (including risks to the womb that can affect further pregnancy), anaesthetic risks and hospital stay. Medical management of first trimester silent miscarriage using misoprostol is another common option that can reduce the risk of bleeding and those associated with surgery. However, the current standard management of using misoprostol for the management of first trimester miscarriage only has a success rate of 70-80%, which is suboptimal.
Recent large studies have shown that adding mifepristone pre-treatment before misoprostol in the management of silent miscarriage can improve the success rates of complete miscarriage after medical management. There are 2 problems with mifepristone. Firstly, it is not widely available in many countries for cultural and religious reasons because it is labelled as an 'abortifacient'. Secondly, it is expensive. One tablet of Mifepristone costs $500 HK dollars. There is a need to look for an alternative to mifepristone.
Letrozole is an aromatase inhibitor which can reduce estrogen levels. Some studies have shown that it can improve the success rate of medical management of silent miscarriage and termination of pregnancy. It is safe, more widely available and cheaper than mifepristone.
This is a randomized double blinded trial comparing the use of mifepristone versus letrozole as pre-treatment in the medical management of first trimester silent miscarriage using misoprostol.

Start Date06 Dec 2024

Sponsor / Collaborator

The University of Hong Kong

[+4]

NCT06689254

/ RecruitingPhase 2IIT

REVERSE: a Randomized Controlled Trial (RCT) to Ameliorate Treatment-resistant Post Traumatic Stress Disorder (PTSD) with Glucocorticoid Receptor (GR) Antagonism

Rationale:
Post-traumatic stress disorder (PTSD) is a psychiatric disorder that can develop in people who have experienced or witnessed a traumatic event. Symptoms of PTSD include flashbacks, nightmares, difficulty sleeping, difficulty concentrating, irritability, and avoidance of people, places, or activities that remind the person of the traumatic event. Even though there are effective treatments (e.g. exposure-based psychotherapies and antidepressants), not all patients respond. Glucocorticoid receptor (GR) antagonism is a potential therapy for the treatment of treatment-resistant post traumatic stress disorder (PTSD) based on the idea that PTSD may be caused or exacerbated by dysregulation of the body's stress response system, and on the results of several small clinical trials. By blocking the actions of cortisol at the GR, it is thought that GR antagonists may be able to reduce the severity of PTSD symptoms and improve treatment outcomes. Randomized controlled trials (RCT) can provide high-quality evidence on treatment efficacy, and optimize evidence-based selection of off-label treatments for patients. Therefore the aim is to investigate whether the psychological and biological sequelae of traumatic stress and PTSD can be targeted by blocking the glucocorticoid receptor (GR) using the generic drug mifepristone in a double blind, placebo controlled RCT.
Objective:
To test the hypothesis that treatment with the GR-antagonist mifepristone is more effective than placebo to reduce PTSD symptom severity in treatment-resistant PTSD.
Main trial endpoints:
Improvement of PTSD symptoms, as measured with the monthly version of the CAPS-5 (Clinician Administered PTSD scale) in patients with treatment-resistant PTSD, 4 weeks after the start of the intervention. Secondary trial endpoints
* PTSD symptom severity as measured with the weekly version of the PCL-5, from baseline till 12 weeks after the start of the intervention (T3).
* Long-term PTSD symptom severity as measured with the CAPS-5, at 12 weeks after the start of the intervention (T3).
* Loss of diagnosis (score of <26 and absence of PTSD criteria with CAPS-5), 4 weeks after the start of the intervention.
* Treatment response (minimum decrease of 10 point on the PCL-5 and CAPS-5 scores) at 1, 4 and 12 weeks after the start of the intervention.
* Other clinical outcomes 1, 4, and 12 weeks after the start the intervention:
* disability (WHO Disability Schedule 2.0; WHO-DAS II),
* sleep (Insomnia Severity Index; ISI),
* subjective stress (Perceived Stress Scale; PSS),
* anxiety symptoms (Beck Anxiety Inventory; BAI),
* depressive symptoms (IDS-SR),
* suicidal ideation and behaviour (Columbia-Suicide Severity Rating Scale).
Trial design:
The experimental protocol consists of a placebo-controlled double-blind RCT with 4 face-to-face meetings:
* baseline (T0, 2,5 hrs);
* post-intervention T1, 8 days after start (1hr);
* post-intervention T2, 4 weeks after start (2hr).
* post-intervention T3, 12 weeks (2hr).
Trial population:
60 adult patients (male/female, 18+ years), with treatment-resistant PTSD (non-response to two evidence-based PTSD treatments, at least one of which is trauma-focused psychotherapy). Intervention Patients are randomized for treatment with the GR antagonist mifepristone (1200 mg/day for 7 days) or matching placebo (daily for 7 days). Study medication will be dispensed during the baseline measurement (T0), and taken once daily for 7 consecutive days. Clinical measurements consist of clinical interviews and questionnaires. During baseline visits a pregnancy test is conducted in woman of child bearing potential (WOCBP), and blood is drawn at T1 to assess mifepristone plasma levels.
Ethical considerations relating to the clinical trial including the expected benefit to the individual subject or group of patients represented by the trial subjects as well as the nature and extent of burden and risks:
Mifepristone has been clinically used for Cushing's syndrome (anti-glucocorticoid effects) and termination of pregnancy (anti-progesterone effects) for several decades. Mifepristone is generally well-tolerated, and several double-blind studies using the identical duration and dose have shown (7 days, 1200 mg) that the safety profile of mifepristone is comparable to that of placebo treatment, and study dropouts due to side effects were higher for placebo (1.6%) than for mifepristone (1.4%). The most common adverse events (AEs) were nausea, headache, dizziness, and a dry mouth and were comparable between the mifepristone and placebo groups. With regard to mifepristone's progesterone receptor activity and its indication for pregnancy termination, WOCBP who do not agree to use a non-hormonal contraceptive method (condom) during the intervention and up to 1 month after the intervention, are strictly excluded from participating in this study.

Start Date15 Nov 2024

Sponsor / Collaborator

Stichting Onderzoek Cancer Center Amsterdam

[+1]

NCT06502158

/ RecruitingPhase 1IIT

Mifepristone Versus Misoprostol for Cervical Preparation Prior to Procedural Abortion at 12 to 16 Weeks' Gestation in an Academic Medical Center: a Randomized Controlled Pilot Trial

The Investigator team hypothesizes that in a randomized trial comparing mifepristone-alone or misoprostol-alone for cervical preparation for procedural abortions at 12 to 16 weeks in hospital-based care, the proportion of patients who achieve successful cervical dilation will be different between the study groups.

Start Date31 Oct 2024

Sponsor / Collaborator

Montefiore Medical Center

100 Clinical Results associated with Mifepristone

100 Translational Medicine associated with Mifepristone

100 Patents (Medical) associated with Mifepristone

7,770

Literatures (Medical) associated with Mifepristone

01 Sep 2025·Neural Regeneration Research

High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

Article

Author: Wu, Hongbin ; Yang, Mengshi ; Deng, Yu ; Liu, Baiyun ; Bai, Miao ; Niu, Fei ; Ge, Qianqian ; Zhuang, Yuan ; Dong, Xinlong ; Zhang, Bin ; Xu, Xiaojian ; Lu, Shenghua ; Li, Hao

JOURNAL/nrgr/04.03/01300535-202509000-00023/figure1/v/2024-12-31T000210Z/r/image-tiff Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury, the fundamental regulatory and functional mechanisms remain insufficiently understood. As potent anti-inflammatory agents, the use of glucocorticoids in traumatic brain injury is still controversial, and their regulatory effects on microglial polarization are not yet known. In the present study, we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action. In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization. Lipopolysaccharide, dexamethasone, RU486 (a glucocorticoid receptor antagonist), and ruxolitinib (a Janus kinase 1 antagonist) were administered. RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone. The Morris water maze, quantitative reverse transcription-polymerase chain reaction, western blotting, immunofluorescence and confocal microscopy analysis, and TUNEL, Nissl, and Golgi staining were performed to investigate our hypothesis. High-throughput sequencing results showed that arginase 1, a marker of M2 microglia, was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at 3 days post–traumatic brain injury. Thus dexamethasone inhibited M1 and M2 microglia, with a more pronounced inhibitory effect on M2 microglia in vitro and in vivo. Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury. Additionally, glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death, and also decreased the density of dendritic spines. A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway. Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia, which plays an anti-inflammatory role. In contrast, inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury. Dexamethasone may exert its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway.

01 Mar 2025·Experimental Neurology

Progesterone receptors regulate susceptibility to spreading depression

Article

Author: Williamson, John ; Baca, Serapio M ; Joshi, Suchitra ; Kapur, Jaideep

Migraine patients often experience sensory symptoms called auras accompanying the headaches. Cortical spreading depression (CSD), a slow-propagating wave of neuroglial depolarization followed by hyperpolarization is proposed to be the neurological mechanism underlying these auras. We have previously found that progesterone regulates susceptibility to migraine through progesterone receptor (PR) activation. Here, we determined if PR signaling also regulates susceptibility to CSD. We used gonadally-intact and ovariectomized, estrogen-primed female mice expressing PRs or lacking them in the brain. CSDs were induced with dural application of KCl (1 M) and recorded using saline-filled glass electrodes placed in the cortex. PRs were modulated using agonist segesterone and antagonist RU-486. PR expression in the somatosensory cortex was evaluated using mice expressing a cre recombinase under the control of Pgr promoter, stereotaxically injected with adeno-associated virus (AAV) serotype 9 encoding flexed GFP. PR expression in excitatory or inhibitory neurons and distinctions in the cortical layer-specific expression were determined. The effect of chemogenetic silencing of PR-expressing somatosensory cortical neurons on CSD susceptibility was also evaluated using AAV9 expressing cre-driven hM4Di. PRs were expressed in the excitatory neurons of the somatosensory cortex. Their expression was stronger in layer 4-6 cortical neurons than in layer 2/3 neurons. PR activation increased CSD frequency and accelerated their propagation speed. In contrast, PR antagonism or their genetic deletion suppressed CSDs. Chemogenetic silencing of PR-expressing somatosensory cortical neurons also reduced the CSD frequency. These findings demonstrate the critical role of progesterone-PR signaling in regulating CSD and enhance our understanding of female hormonal regulation of migraine pathophysiological mechanisms.

01 Feb 2025·Neuroscience

Progesterone and allopregnanolone facilitate excitatory synaptic transmission in the infralimbic cortex via activation of membrane progesterone receptors

Article

Author: Buynack, Lauren M ; Rahaei, Nima ; Movasseghi, Yasamin ; Kires, Lukas ; Chapman, C Andrew

Estrogens and progesterone can have rapid effects on neuronal function and can modify the use of spatial navigation strategies dependent upon the prefrontal cortex, striatum, and hippocampus. Here, we assessed the effects of 17β-estradiol (E2), progesterone, and its metabolite allopregnanolone, on evoked excitatory postsynaptic potentials in the infralimbic region of the female rat prefrontal cortex. Field excitatory postsynaptic potentials (fEPSPs) evoked by stimulation of layer I were first characterized by recording responses at multiple depths between the cortical surface and the underlying white matter. Current source density analysis showed that the short-latency negative component was generated by activation of synaptic currents within layer I, and that putative polysynaptic responses were generated in layers III to V. The amplitude of evoked field EPSPs in layer I was not significantly affected by 20 min application of 17β-estradiol (10 nM), but both 100 nM progesterone and 1 µM allopregnanolone caused lasting increases in field EPSP amplitude. The effects of progesterone were not blocked by the nuclear progesterone receptor antagonist RU486 (1 µM). Both progesterone and allopregnanolone are known to activate membrane progesterone receptors, and we found that the membrane progesterone receptor agonist Org OD 02-0 facilitated EPSPs, and also occluded further increases induced by either progesterone or allopregnanolone. These results provide evidence that both progesterone and allopregnanolone facilitate synaptic responses in layer I of the infralimbic cortex by activating membrane progesterone receptors.

232

News (Medical) associated with Mifepristone

31 Dec 2024

·pipelinereview.com

Corcept Submits New Drug Application for Relacorilant as a Treatment for Patients With Hypercortisolism

REDWOOD CITY, CA, USA I December 30, 2024 I Corcept Therapeutics Incorporated (NASDAQ: CORT), a commercial-stage company engaged in the discovery and development of medications to treat severe endocrinologic, oncologic, metabolic and neurologic disorders by modulating the effects of the hormone cortisol, has submitted a new drug application (NDA) to the U.S. Food and Drug Administration for its proprietary, selective cortisol modulator, relacorilant, to treat patients with endogenous hypercortisolism (Cushing’s syndrome). Corcept’s NDA is based on positive results from the pivotal GRACE trial and confirmatory evidence from the Phase 3 GRADIENT and long-term extension studies and a Phase 2 study in hypercortisolism. Patients in these studies who received relacorilant experienced improvements in a wide array of hypercortisolism’s signs and symptoms, with an acceptable safety burden. Notably, there were no instances of drug-induced adrenal insufficiency, hypokalemia or QT prolongation – serious adverse events that can arise in patients taking currently approved medications – and no adverse events associated with activity at the progesterone receptor, such as endometrial thickening or vaginal bleeding. “Relacorilant’s combination of efficacy and safety give it the potential to become the standard of care for the medical treatment of patients with hypercortisolism,” said Joseph Belanoff, MD, Corcept’s Chief Executive Officer. “Our commitment to the health of patients with hypercortisolism is unwavering. We are optimistic that relacorilant will be of great benefit to them.” About Relacorilant Relacorilant is a selective cortisol modulator that binds to the glucocorticoid receptor but not to the body’s other hormone receptors. Corcept is studying relacorilant in a variety of serious disorders in addition to endogenous hypercortisolism (Cushing’s syndrome), including ovarian, adrenal and prostate cancer. Relacorilant is proprietary to Corcept and is protected by composition of matter, method of use and other patents. Relacorilant has orphan drug designation in the United States and the European Union for the treatment of Cushing’s syndrome. About Hypercortisolism (Cushing’s Syndrome) Hypercortisolism is caused by excessive activity of the hormone cortisol. Symptoms vary, but most patients experience one or more of the following manifestations: hypertension, central obesity, elevated blood sugar and difficult-to-control type 2 diabetes, severe fatigue and weak muscles. Irritability, anxiety, depression and cognitive disturbances are common. Hypercortisolism can affect every organ system and can be lethal if not treated effectively. About Corcept Therapeutics For over 25 years, Corcept’s focus on cortisol modulation and its potential to treat patients with a wide variety of serious disorders has led to the discovery of more than 1,000 proprietary selective cortisol modulators. Corcept is conducting advanced clinical trials in patients with hypercortisolism, solid tumors, ALS and liver disease. In February 2012, the company introduced Korlym ® , the first medication approved by the U.S. Food and Drug Administration for the treatment of patients with endogenous hypercortisolism. Corcept is headquartered in Redwood City, California. For more information, visit Corcept.com. SOURCE: Corcept Therapeutics

Clinical ResultOrphan DrugNDADrug ApprovalPhase 2

30 Dec 2024

·ir.corcept.com

Corcept Submits New Drug Application for Relacorilant as a Treatment for Patients With Hypercortisolism

REDWOOD CITY, Calif.--(BUSINESS WIRE)--Dec. 30, 2024-- Corcept Therapeutics Incorporated (NASDAQ: CORT), a commercial-stage company engaged in the discovery and development of medications to treat severe endocrinologic, oncologic, metabolic and neurologic disorders by modulating the effects of the hormone cortisol, has submitted a new drug application (NDA) to the U.S. Food and Drug Administration for its proprietary, selective cortisol modulator, relacorilant, to treat patients with endogenous hypercortisolism (Cushing’s syndrome). Corcept’s NDA is based on positive results from the pivotal GRACE trial and confirmatory evidence from the Phase 3 GRADIENT and long-term extension studies and a Phase 2 study in hypercortisolism. Patients in these studies who received relacorilant experienced improvements in a wide array of hypercortisolism’s signs and symptoms, with an acceptable safety burden. Notably, there were no instances of drug-induced adrenal insufficiency, hypokalemia or QT prolongation – serious adverse events that can arise in patients taking currently approved medications – and no adverse events associated with activity at the progesterone receptor, such as endometrial thickening or vaginal bleeding. “Relacorilant’s combination of efficacy and safety give it the potential to become the standard of care for the medical treatment of patients with hypercortisolism,” said Joseph Belanoff, MD, Corcept’s Chief Executive Officer. “Our commitment to the health of patients with hypercortisolism is unwavering. We are optimistic that relacorilant will be of great benefit to them.” About Relacorilant Relacorilant is a selective cortisol modulator that binds to the glucocorticoid receptor but not to the body's other hormone receptors. Corcept is studying relacorilant in a variety of serious disorders in addition to endogenous hypercortisolism (Cushing’s syndrome), including ovarian, adrenal and prostate cancer. Relacorilant is proprietary to Corcept and is protected by composition of matter, method of use and other patents. Relacorilant has orphan drug designation in the United States and the European Union for the treatment of Cushing’s syndrome. About Hypercortisolism (Cushing’s Syndrome) Hypercortisolism is caused by excessive activity of the hormone cortisol. Symptoms vary, but most patients experience one or more of the following manifestations: hypertension, central obesity, elevated blood sugar and difficult-to-control type 2 diabetes, severe fatigue and weak muscles. Irritability, anxiety, depression and cognitive disturbances are common. Hypercortisolism can affect every organ system and can be lethal if not treated effectively. About Corcept Therapeutics For over 25 years, Corcept’s focus on cortisol modulation and its potential to treat patients with a wide variety of serious disorders has led to the discovery of more than 1,000 proprietary selective cortisol modulators. Corcept is conducting advanced clinical trials in patients with hypercortisolism, solid tumors, ALS and liver disease. In February 2012, the company introduced Korlym®, the first medication approved by the U.S. Food and Drug Administration for the treatment of patients with endogenous hypercortisolism. Corcept is headquartered in Redwood City, California. For more information, visit Corcept.com. Forward-Looking Statements Statements in this press release, other than statements of historical fact, are forward-looking statements based on our current plans and expectations and are subject to risks and uncertainties that might cause our actual results to differ materially from those such statements express or imply. These risks and uncertainties are set forth in our SEC filings, which are available at our website and the SEC’s website. In this press release, forward-looking statements include statements concerning: the results of our Phase 2, GRACE, GRADIENT, and long-term extension studies; relacorilant’s efficacy, safety and other clinical attributes and its potential to receive regulatory approval and become a standard-of-care treatment for patients with endogenous hypercortisolism; regulatory oversight of relacorilant and the scope, pace and outcome of its NDA submission; relacorilant’s acceptance and use by physicians and patients and its commercial prospects; and the scope and protective power of relacorilant’s orphan drug designation and our intellectual property. We disclaim any intention or duty to update forward-looking statements made in this press release. View source version on businesswire.com: https://www.businesswire.com/news/home/20241230947567/en/ Investor inquiries: ir@corcept.com Media inquiries: communications@corcept.com www.corcept.com Source: Corcept Therapeutics Incorporated

Clinical ResultOrphan DrugNDAPhase 2Phase 3

16 Dec 2024

·www.businesswire.com

Corcept’s Phase 3 Long-Term Extension Study of Relacorilant Demonstrated Durable Cardiometabolic Improvements in Patients with Hypercortisolism

REDWOOD CITY, Calif.--( BUSINESS WIRE )--Corcept Therapeutics Incorporated (NASDAQ: CORT), a commercial-stage company engaged in the discovery and development of medications to treat severe endocrinologic, oncologic, metabolic and neurologic disorders by modulating the effects of the hormone cortisol, presented results from its Phase 3 long-term, open-label extension study of relacorilant to treat patients with endogenous hypercortisolism (Cushing’s syndrome) at the WCIRDC. The results from this study demonstrated that patients treated with relacorilant experienced clinically meaningful and durable cardiometabolic improvements and relacorilant was well-tolerated, with a treatment duration of up to six years. The Phase 3 long-term extension study enrolled 116 patients who had previously completed either Corcept’s Phase 3 GRACE or GRADIENT studies or its Phase 2 study in hypercortisolism. Patients experienced further improvement in blood pressure while maintaining response in other cardiometabolic measures, such as glycemic control and body weight. Consistent with its known safety profile, relacorilant was well-tolerated with a treatment duration of up to six years. At month 24 of the study, patients exhibited clinically meaningful and statistically significant reductions in mean systolic blood pressure (10.0 mm Hg; p-value: 0.012) and mean diastolic blood pressure (7.3 mm Hg; p-value: 0.016), compared to their measurement at entry into the long-term extension study. Patients who resumed receiving relacorilant in the extension study, after being switched to placebo in the randomized-withdrawal phase of the GRACE study, experienced both a reversal of the deterioration they exhibited while receiving placebo and additional improvement beyond their blood pressure measurement at entry into the randomized portion of the study. To ensure accuracy, blood pressure was measured by 24-hour ambulatory blood pressure monitoring. Dr. Richard Auchus, MD, PhD, Professor of Internal Medicine in the Division of Metabolism, Endocrinology & Diabetes at the University of Michigan and Chief of the Endocrinology & Metabolism Section at the Ann Arbor VA Medical Center, presented the long-term extension results at WCIRDC. “People living with hypercortisolism are at risk of serious cardiometabolic comorbidities, including hypertension and hyperglycemia. These long-term data demonstrate significant improvements across a broad set of signs and symptoms of hypercortisolism without the toxicities observed with current treatment options. It is especially encouraging to see data from patients treated for up to six years that show progressive reductions in blood pressure, maintenance of cardiometabolic improvements, and long-term drug tolerability,” said Dr. Auchus. “The positive results from the long-term extension study of relacorilant are consistent with findings from our GRACE, GRADIENT and Phase 2 studies. These data will support relacorilant’s new drug application (NDA), which we plan to submit this month,” said Bill Guyer, PharmD, Corcept’s Chief Development Officer. “Relacorilant’s strong efficacy and safety profile positions the medication to become a new standard of care in treating patients with hypercortisolism.” The presentation at WCIRDC is available here . About Relacorilant Relacorilant is a selective cortisol modulator that binds to the glucocorticoid receptor but not to the body's other hormone receptors. Corcept is studying relacorilant in a variety of serious disorders in addition to endogenous hypercortisolism (Cushing’s syndrome), including ovarian, adrenal and prostate cancer. Relacorilant is proprietary to Corcept and is protected by composition of matter, method of use and other patents. Relacorilant has orphan drug designation in the United States and the European Union for the treatment of Cushing’s syndrome. About Hypercortisolism (Cushing’s Syndrome) Hypercortisolism is caused by excessive activity of the hormone cortisol. Symptoms vary, but most patients experience one or more of the following manifestations: hypertension, central obesity, elevated blood sugar and difficult-to-control type 2 diabetes, severe fatigue and weak muscles. Irritability, anxiety, depression and cognitive disturbances are common. Hypercortisolism can affect every organ system and can be lethal if not treated effectively. About Corcept Therapeutics For over 25 years, Corcept’s focus on cortisol modulation and its potential to treat patients with a wide variety of serious disorders has led to the discovery of more than 1,000 proprietary selective cortisol modulators. Corcept is conducting advanced clinical trials in patients with hypercortisolism, solid tumors, ALS and liver disease. In February 2012, the company introduced Korlym ® , the first medication approved by the U.S. Food and Drug Administration for the treatment of patients with endogenous hypercortisolism. Corcept is headquartered in Redwood City, California. For more information, visit Corcept.com. Forward-Looking Statements Statements in this press release, other than statements of historical fact, are forward-looking statements based on our current plans and expectations and are subject to risks and uncertainties that might cause our actual results to differ materially from those such statements express or imply. These risks and uncertainties are set forth in our SEC filings, which are available at our website and the SEC’s website. In this press release, forward-looking statements include statements concerning: relacorilant, including its clinical attributes and potential to receive regulatory approval and become a standard-of-care treatment for patients with endogenous hypercortisolism or any other disorder; regulatory oversight of relacorilant and the scope, pace and outcome of its NDA submission; relacorilant’s acceptance and use by physicians and patients and its commercial prospects; and the scope and protective power of relacorilant’s orphan drug designation and our intellectual property. We disclaim any intention or duty to update forward-looking statements made in this press release.

Clinical ResultPhase 2Orphan DrugDrug ApprovalPhase 3

100 Deals associated with Mifepristone

External Link

KEGG	Wiki	ATC	Drug Bank
D00585	Mifepristone	G03XB01	DB00834

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Induced Abortion	AU	MS Health Pty Ltd.	29 Aug 2012
Cushing Syndrome	US	Corcept Therapeutics, Inc.	17 Feb 2012
Induced termination of pregnancy in second trimester	US	Danco Laboratories LLC	28 Sep 2000
Contraception	CN	Hongjian Pharmaceutical (Shanghai) Co., Ltd.	-

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Uterine Fibroids	Phase 2	CN	Hubei Gedian Humanwell Pharmaceutical Co., Ltd.	19 Oct 2012
Hemorrhage	Phase 1	IL	BioPro Medical Ltd	01 Apr 2009
Leiomyoma	Phase 1	IL	BioPro Medical Ltd	01 Apr 2009
Endogenous Cushing Syndrome	Phase 1	US	Corcept Therapeutics, Inc.	01 Dec 2007
Weight Gain	Phase 1	IN	Corcept Therapeutics, Inc.	01 Mar 2007
Depressive Disorder, Major	Phase 1	US	Corcept Therapeutics, Inc.	01 Sep 2004
Pituitary ACTH Hypersecretion	Discovery	US	Corcept Therapeutics, Inc.	01 Nov 2010
Affective Disorders, Psychotic	Discovery	US	Corcept Therapeutics, Inc.	01 Mar 2008
Depressive Disorder, Major	Discovery	US	Corcept Therapeutics, Inc.	01 Sep 2004
Alzheimer Disease	Discovery	US	Corcept Therapeutics, Inc.	01 Apr 2003

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


CATALYST (BusinessWire) Manual	Phase 4	Diabetes Mellitus \| Cushing Syndrome	136	Korlym	(ojzxvddczy) = xegothlquo ppaoovnhep (ixfibahzgs ) Met	Positive	12 Dec 2024
				Placebo	(ojzxvddczy) = mqsusoxqby ppaoovnhep (ixfibahzgs ) Met
NCT03913104 (CTgov)	Phase 4	Abortion, Spontaneous	536	Mifepristone	ulruvclmgc(zwvhsjkygt) = ghxvydmioo rubhlxtwvf (mcrqeanqwy, pkfqqtrnlj - uxjnvlsstm) View more	-	14 Aug 2024
NCT05097326 (MiLI, CTgov)	Phase 3	-	30	Mifepristone (Mifepristone)	facmtvuqzw(uyjjkbeufv) = lyrwqambkg asevsakopo (onibuuidju, wcwptkjrrx - dneaskvahq) View more	-	31 Jul 2024
				Misoprostol (Misoprostol)	facmtvuqzw(uyjjkbeufv) = fbofbaxqud asevsakopo (onibuuidju, jonmhfwdny - jbfwddzyqv) View more
ENDO2024	Not Applicable	Diabetes Mellitus, Type 2 hypercortisolism	-	Mifepristone 300 mg/day	bhkdovwhuj(pqaecezuyz) = Upon discontinuation, the patient's glycemic control quickly deteriorated (CGM TIR 3%, HbA1c 10.2%, average glucose 286 mg/dL), with increased insulin use, weight gain, and reintroduction of 2 antihyperglycemic medications and 2 antihypertensive medications wrbbhsagqb (vxzzzcjvsp )	Positive	01 Jun 2024
				Placebo
ENDO2024	Not Applicable	Cushing Syndrome	-	Mifepristone 300 mg/day	qwudwspbiu(enpsdtsegp) = An 82-year-old woman presented to the emergency department after five days of nausea, abdominal pain, palpitations, and reduced oral intake. She was found to have severe hypokalemia (potassium 1.8 mEq/L, normal 3.5 - 5.0 mEq/L) vqcunysmjm (gesietacpt )	-	01 Jun 2024
NCT02788981 (CTgov)	Phase 2	-	29	nab-paclitaxel+Mifepristone (Nab-Paclitaxel+Mifepristone)	(jbqmnhfpdo) = aiqmcjhkph nvhtadjldx (rdayebimeo, cceaotoeso - cibzxanrjb) View more	-	16 Feb 2024
				Placebo+nab-paclitaxel (Nab-Paclitaxel+Placebo)	(jbqmnhfpdo) = iqdnybylrj nvhtadjldx (rdayebimeo, owmfhqsdjt - zyghflvtxt) View more
THU621 (ENDO2023)	Not Applicable	Cushing Syndrome Late Night Salivary Cortisol(LNSC) \| Dexamethasone Suppression Test(DST) \| 24-hr Urinary-Free Cortisol(UFC)	1	Mifepristone 300mg daily	jdidcvtcco(skbtugjuvb) = Her only side effect was mild nausea that later resolved goxdlcehxg (oufbakpsom )	Positive	05 Oct 2023
				Mifepristone up to 1200mg daily
NCT03520439 (Pubmed \| JAMA Netw Open)	Phase 2/3	Adenomyosis	134	Mifepristone 10 mg	eaoadvhyzk(vncmiakhpg) = yqqbwxjlme zvzrdaajyf (irvwbfuwia ) View more	Positive	01 Jun 2023
				Placebo	eaoadvhyzk(vncmiakhpg) = rsqncrkfrb zvzrdaajyf (irvwbfuwia ) View more
NCT02243709 (CTgov)	Phase 1/2	Alcohol Use Disorder	32	Mifepristone 600-mg/day or placebo for a week	dgvklxwbal(wtoqyztajt) = thjleloerl klkmbbudxx (ovwxvqdpgc, lbkivltnzg - qeokqujiht) View more	-	01 Jun 2023
NCT03225547 (ASCO 12023 \| ASCO 22023) Manual	Phase 2	HER2-negative breast cancer HER2 Negative	18	mifepristone 300 mg+pembrolizumab 200 mg	(smsnqocuuu) = yeodfbaaic zehftpkvzg (szvyemehgl ) View more	Positive	26 May 2023

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Understand key drug designations in just a few clicks with Synapse.

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Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis