Naji Gehchan, MD, MBA, Chief Medical and Development Officer at Kyverna Therapeutics, discusses primary analysis of KYV-101 for the treatment of stiff person syndrome (SPS).

SPS is a progressive neuromuscular condition caused by increased muscle activity due to decreased inhibition of the central nervous system. Symptoms may include extreme muscle stiffness, rigidity and painful spasms in the trunk and limbs. People with SPS often have heightened sensitivity to noise, sudden movements, and emotional distress, which can set off muscle spasms. The syndrome affects twice as many women as men. It is thought to have an autoimmune component and is often associated with diabetes, as well as other autoimmune diseases.

Miv-cel (mivocabtagene autoleucel, KYV-101) is a fully human, autologous CD19 CAR T-cell therapy designed to target anti-CD19, a protein involved in various types of autoimmune diseases. Positive primary analysis results from its registrational trial, KYSA-8 clinical trial of miv-cel (mivocabtagene autoleucel, KYV-101) in SPS was presented at the 2026 American Academy of Neurology Annual Meeting (AAN 2026).

KYSA-8 is a single-arm registrational phase 2 study evaluating KYV-101 in patients with SPS. The primary endpoints are the change from baseline in the Timed 25-Foot Walk (T25FW) at 16 weeks and the incidence and severity of adverse events. Secondary endpoints measuring disability, stiffness, hypersensitivity, and mobility include the Modified Rankin Scale (mRS), Distribution-of-stiffness Index (DSI), Heightened Sensitivity Scale (HSS), and Hauser Ambulation Index (HAI), respectively. A total of 26 patients who had an inadequate response to off-label immunomodulatory treatment options received a single dose of 1×108 KYV-101 CAR T cells. The median follow-up was 6.5 months after infusion.

The trial met its primary endpoint, demonstrating a statistically significant improvement in the T25FW at week 16, with a median improvement of 46% from baseline, regardless of baseline patient- and disease-related characteristics. 81% of patients achieved clinically meaningful improvement, with nearly 1/3 of all patients walking at the speed of healthy adults by week 16. Of the 12 patients requiring a walking aid at baseline, 67% no longer needed walking assistance at week 16. Additionally, all patients remained free of chronic immunotherapies at week 16 and through last follow-up.

The trial also met all secondary endpoints with significant mean improvements in mRS, HAI, DSI, and HSS of -0.8, -1.6, -1.5, and -3.2 points, respectively.

In exploratory endpoints, sustained clinical benefit associated with deep, transient B-cell depletion and broad immune reset, significant reductions in GAD65-autoantibody titers associated with SPS, and improvements in physical and mental functioning, including a more than 4-fold improvement over the minimal clinically important change in the 6-Minute Walk Test (6-MWT), and normalization toward healthy population benchmarks across the 36-Item Short Form Health Survey (SF-36) domains, were observed.

KYV-101 was well tolerated with no high-grade cytokine release syndrome (CRS) or immune effector cell-associated neurotoxicity syndrome (ICANS) observed. Grade 3/4 neutropenia, a known adverse event associated with lymphodepletion and CAR T-cell therapy, was observed in four patients and was manageable. Serious treatment-related adverse events occurred in three patients, all of which resolved fully without sequelae.

CHAPTERS
Introduction 00:00
Stiff Person Syndrome Overview 00:34
KYSA-8 Clinical Trial 1:59
Measuring Disability 3:45
Rise in Disease Awareness 4:50

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Hans Katzberg, MD, Assistant Professor of Neurology at the University of Toronto and Neurologist at Toronto General Hospital, discusses post hoc analyses from the ADHERE clinical trial in chronic inflammatory demyelinating polyneuropathy (CIDP).

CIDP is a neurological disorder that causes progressive weakness and impaired sensory function in the legs and arms. Symptoms often include tingling or numbness, weakness of the arms and legs, loss of deep tendon reflexes, fatigue, and abnormal sensations. Other symptoms may include pain, dysphagia, and double vision. CIDP is thought to be caused by the immune system mistakenly attacking and damaging the myelin sheath of the peripheral nerves. CIDP is closely related to Guillain-Barre syndrome.

At the 2026 American Academy of Neurology Annual Meeting (ANN 2026), post hoc analyses of the ADHERE (NCT04281472) and open-label extension ADHERE+ (NCT04280718) clinical trials evaluating the impact of subcutaneous efgartigimod PH20 on treatment-naïve patients with CIDP was presented. Efgartigimod is a human immunoglobulin (Ig) G1 antibody Fc fragment that blocks the neonatal Fc receptor, thus decreasing IgG recycling and reducing IgGs. 

Patients with active CIDP received weekly efgartigimod PH20 subcutaneous 1000 mg (stage-A) for 12 or fewer weeks. Those with confirmed evidence of clinical improvement entered stage-B and were randomized to weekly efgartigimod PH20 or placebo for 48 or fewer weeks. Participants with clinical deterioration in stage-B or who completed ADHERE could enter ADHERE+. The primary endpoint of ADHERE stage-A was the percentage of participants with evidence of clinical improvement. Changes from stage-A baseline to stage-A last assessment in adjusted Inflammatory Neuropathy Cause and Treatment (aINCAT), Inflammatory Rasch-built Overall Disability Scale (I-RODS), and grip strength scores were assessed.

Of the 322 participants enrolled in ADHERE, 24 were treatment-naïve. During stage-A (week 12 or before), 87.5% of treatment-naïve participants had confirmed evidence of clinical improvement, compared with 64.8% across the remaining study population. Time to initial confirmed evidence of clinical improvement among treatment-naïve participants was 39.5 days. Improvements exceeding the minimal clinically important difference were reported from stage-A baseline to stage-A last assessment across mean aINCAT, I-RODS, and dominant hand grip strength scores in treatment-naïve participants.

CHAPTERS
Introduction 00:00
CIDP Overview 00:24
Role of Antibodies 1:35
Diagnostic Challenges 2:10
Signs and Symptoms 2:52
ADHERE Clinical Trial 3:20

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Amol Sura, MD, Foster Center for Ocular Immunology, Dept of Ophthalmology, Duke University, Durham, North Carolina, discusses the diagnosis and management of plasminogen deficiency, a rare condition in which the eyes are first affected, but it manifests in mucous membranes throughout the body.

“The eyes are a window into the health of the entire body,” said Dr. Sura, and that is precisely the case for patients with plasminogen deficiency type 1 (PLGD-1). For this rare, inherited condition, the first symptom observed is the growth of ligneous or wood-like lesions on the surface of the eye or eyelid (in about 80% of patients, first seen at ages 9–10 months). It is often characterized as ligneous conjunctivitis.

If left untreated, PLGD-1 may result in severe—even life-threatening—complications, affecting mucous membranes in many other areas of the body, including the respiratory tract, central nervous system, gingiva, and genitourinary tract. Vision loss, tooth loss, and other serious outcomes have been reported.

In this homozygous condition involving the PLG gene, the plasminogen protein is defective; it cannot effectively perform its intended function of breaking down fibrin. The result is the formation of fibrin clots appearing as ligneous growths or pseudomembranes. Once removed, these lesions reappear, and this should tip off the physician (most often an ophthalmologist) that something systemic is the cause.

The diagnosis of PLGD-1 is straightforward: A blood test showing decreased plasminogen activity levels is confirmatory. A genetic test is not necessary.

In the past, management of PLGD-1 was through the use of off-label therapies, including heparin eyedrops, immunologics, and plasma infusions. A form of intravenous human plasminogen was approved by the U.S. Food and Drug Administration in 2021, and this is considered the standard of care today. With this therapy, plasminogen plasma levels can be restored, lowering the risk of new fibrin clots throughout the body.

For newly diagnosed patients, the best advice for caregivers is to establish a relationship with a hematologist, who will serve as principal care provider. Although a multidisciplinary care team is required (e.g., ophthalmology, obstetrics/gynecology, dentistry), the need for other specific providers will depend on the other organs or sites affected.

Dr. Sura believes that PLDG-1 is underdiagnosed, but with increasing awareness, and the availability of effective treatment, diagnosis and management of these patients can be improved today.

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Amol Sura, MD, Foster Center for Ocular Immunology, Dept of Ophthalmology, Duke University, Durham, North Carolina, discusses the diagnosis and management of plasminogen deficiency, a rare condition in which the eyes are first affected, but it manifests in mucous membranes throughout the body.

“The eyes are a window into the health of the entire body,” said Dr. Sura, and that is precisely the case for patients with plasminogen deficiency type 1 (PLGD-1). For this rare, inherited condition, the first symptom observed is the growth of ligneous or wood-like lesions on the surface of the eye or eyelid (in about 80% of patients, first seen at ages 9–10 months). It is often characterized as ligneous conjunctivitis.

If left untreated, PLGD-1 may result in severe—even life-threatening—complications, affecting mucous membranes in many other areas of the body, including the respiratory tract, central nervous system, gingiva, and genitourinary tract. Vision loss, tooth loss, and other serious outcomes have been reported.

In this homozygous condition involving the PLG gene, the plasminogen protein is defective; it cannot effectively perform its intended function of breaking down fibrin. The result is the formation of fibrin clots appearing as ligneous growths or pseudomembranes. Once removed, these lesions reappear, and this should tip off the physician (most often an ophthalmologist) that something systemic is the cause.

The diagnosis of PLGD-1 is straightforward: A blood test showing decreased plasminogen activity levels is confirmatory. A genetic test is not necessary.

In the past, management of PLGD-1 was through the use of off-label therapies, including heparin eyedrops, immunologics, and plasma infusions. A form of intravenous human plasminogen was approved by the U.S. Food and Drug Administration in 2021, and this is considered the standard of care today. With this therapy, plasminogen plasma levels can be restored, lowering the risk of new fibrin clots throughout the body.

For newly diagnosed patients, the best advice for caregivers is to establish a relationship with a hematologist, who will serve as principal care provider. Although a multidisciplinary care team is required (e.g., ophthalmology, obstetrics/gynecology, dentistry), the need for other specific providers will depend on the other organs or sites affected.

Dr. Sura believes that PLDG-1 is underdiagnosed, but with increasing awareness, and the availability of effective treatment, diagnosis and management of these patients can be improved today.

CHAPTERS
Introduction 00:00
PLGD Overview 1:11
Diagnostic Pathway 2:23
Role of Genetic Testing 3:25
Serious Complications 4:00
Advice for Newly Diagnosed Patients 4:42
Take Home Message 6:07

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Angela Zhu, MD, is an Ophthalmologist and Clinical Assistant Professor, Pediatric & Adult Cornea/Cataract/External Diseases, at Bascom Palmer Eye Institute in Miami. In this interview with
CheckRare, Dr. Zhu describes some of the key features of plasminogen deficiency and why ophthalmologists are often the healthcare providers who begin the process toward diagnosis.

Plasminogen deficiency type 1 (PLGD-1) is a rare genetic disorder in which the body fails to make adequate quantities of plasminogen, the molecule responsible for protection against abnormal fibrin clotting. It generally manifests initially (in about 80%) as ligneous conjunctivitis, in which thick membraneous lesions (from from fibrin accumulation) develop on the surface of the eye and in the eyelid. As a result, Dr. Zhu said, ophthalmologists are usually the first healthcare provider to see the patient and start the diagnostic journey.

Even though the ligneous lesions on the eye are generally the first symptom in young patients, PLGD-1 can present in many different ways (and in virtually any organ system with mucous membranes). However, fibrin accumulations in internal organs or tissue may be harder to detect.
The diagnosis may not be obvious, especially if the telltale ophthalmologic sign is misread as common infectious conjunctivitis. Patients with PLGD1 can have multiple other symptoms that wax and wane, said Dr. Zhu, and “we need to educate providers about the disease and how it can present. It is underdiagnosed and underrecognized.”

In patients with ligneous conjunctivitis, these fibrous lesions can first be mistaken for discharge, which is common in infectious conjunctivitis. But it doesn’t respond to treatment, unlike viral or bacterial causes of conjunctivitis would. Once the ligneous lesion is removed from the eye, because the plasminogen deficiency is not remedied, it will likely form again.

In the case of these eye lesions or conjunctivitis that doesn’t resolve with antiallergy, steroidal, or antiviral treatment, or grow back after removal, Dr. Zhu stated that laboratory testing for plasminogen activity and antigen testing should be the next step. It will diagnose the condition. “But it could take months before a provider makes the connection [that PLGD1 is the cause].”

The extravascular, fibrin-rich lesions that appear anywhere there is mucous membranes can cause serious or even life-threatening complications. For example, the growths could cause airway obstruction, renal failure if the kidney is involved, chronic hearing loss, or blindness.

“Prior to 2023, we didn’t have an FDA-approved treatment,” she noted. Fresh frozen plasma infusions, which had low plasminogen concentrations, were the mainstay. In 2023, the FDA approved a human-derived plasminogen infusion, which effectively raises plasminogen blood concentrations and ensures adequate plasminogen activity. Plasminogen infusions must be given every two to four days. Five years after initializing therapy, patients have remained free of new lesions, said Dr. Zhu.

The adverse events associated with the infusion include infusion-site reactions, bloating, nausea, and fatigue. She also related that there is a theoretical risk for introduction of infection (as it is a blood product). The fibrin-rich growths can suddenly slough off with therapy, and this could potentially cause unique problems (e.g., a sizeable lesion in the airway breaking off) or bleeding.

CHAPTERS
Introduction 00:00
Plasminogen Deficiency Type 1 Overview 00:56
Diagnostic Odyssey 2:36
Disease Complications 6:08

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Angela Zhu, MD, is an Ophthalmologist and Clinical Assistant Professor, Pediatric & Adult Cornea/Cataract/External Diseases, at Bascom Palmer Eye Institute in Miami. In this interview with
CheckRare, Dr. Zhu describes some of the key features of plasminogen deficiency and why ophthalmologists are often the healthcare providers who begin the process toward diagnosis.

Plasminogen deficiency type 1 (PLGD-1) is a rare genetic disorder in which the body fails to make adequate quantities of plasminogen, the molecule responsible for protection against abnormal fibrin clotting. It generally manifests initially (in about 80%) as ligneous conjunctivitis, in which thick membraneous lesions (from from fibrin accumulation) develop on the surface of the eye and in the eyelid. As a result, Dr. Zhu said, ophthalmologists are usually the first healthcare provider to see the patient and start the diagnostic journey.

Even though the ligneous lesions on the eye are generally the first symptom in young patients, PLGD-1 can present in many different ways (and in virtually any organ system with mucous membranes). However, fibrin accumulations in internal organs or tissue may be harder to detect.
The diagnosis may not be obvious, especially if the telltale ophthalmologic sign is misread as common infectious conjunctivitis. Patients with PLGD1 can have multiple other symptoms that wax and wane, said Dr. Zhu, and “we need to educate providers about the disease and how it can present. It is underdiagnosed and underrecognized.”

In patients with ligneous conjunctivitis, these fibrous lesions can first be mistaken for discharge, which is common in infectious conjunctivitis. But it doesn’t respond to treatment, unlike viral or bacterial causes of conjunctivitis would. Once the ligneous lesion is removed from the eye, because the plasminogen deficiency is not remedied, it will likely form again.

In the case of these eye lesions or conjunctivitis that doesn’t resolve with antiallergy, steroidal, or antiviral treatment, or grow back after removal, Dr. Zhu stated that laboratory testing for plasminogen activity and antigen testing should be the next step. It will diagnose the condition. “But it could take months before a provider makes the connection [that PLGD1 is the cause].”

The extravascular, fibrin-rich lesions that appear anywhere there is mucous membranes can cause serious or even life-threatening complications. For example, the growths could cause airway obstruction, renal failure if the kidney is involved, chronic hearing loss, or blindness.

“Prior to 2023, we didn’t have an FDA-approved treatment,” she noted. Fresh frozen plasma infusions, which had low plasminogen concentrations, were the mainstay. In 2023, the FDA approved a human-derived plasminogen infusion, which effectively raises plasminogen blood concentrations and ensures adequate plasminogen activity. Plasminogen infusions must be given every two to four days. Five years after initializing therapy, patients have remained free of new lesions, said Dr. Zhu.

The adverse events associated with the infusion include infusion-site reactions, bloating, nausea, and fatigue. She also related that there is a theoretical risk for introduction of infection (as it is a blood product). The fibrin-rich growths can suddenly slough off with therapy, and this could potentially cause unique problems (e.g., a sizeable lesion in the airway breaking off) or bleeding.

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Angela Zhu, MD, is an Ophthalmologist and Clinical Assistant Professor, Pediatric & Adult Cornea/Cataract/External Diseases, at Bascom Palmer Eye Institute in Miami. In this interview with
CheckRare, Dr. Zhu describes some of the key features of plasminogen deficiency and why ophthalmologists are often the healthcare providers who begin the process toward diagnosis.

Plasminogen deficiency type 1 (PLGD-1) is a rare genetic disorder in which the body fails to make adequate quantities of plasminogen, the molecule responsible for protection against abnormal fibrin clotting. It generally manifests initially (in about 80%) as ligneous conjunctivitis, in which thick membraneous lesions (from from fibrin accumulation) develop on the surface of the eye and in the eyelid. As a result, Dr. Zhu said, ophthalmologists are usually the first healthcare provider to see the patient and start the diagnostic journey.

Even though the ligneous lesions on the eye are generally the first symptom in young patients, PLGD-1 can present in many different ways (and in virtually any organ system with mucous membranes). However, fibrin accumulations in internal organs or tissue may be harder to detect.
The diagnosis may not be obvious, especially if the telltale ophthalmologic sign is misread as common infectious conjunctivitis. Patients with PLGD1 can have multiple other symptoms that wax and wane, said Dr. Zhu, and “we need to educate providers about the disease and how it can present. It is underdiagnosed and underrecognized.”

In patients with ligneous conjunctivitis, these fibrous lesions can first be mistaken for discharge, which is common in infectious conjunctivitis. But it doesn’t respond to treatment, unlike viral or bacterial causes of conjunctivitis would. Once the ligneous lesion is removed from the eye, because the plasminogen deficiency is not remedied, it will likely form again.

In the case of these eye lesions or conjunctivitis that doesn’t resolve with antiallergy, steroidal, or antiviral treatment, or grow back after removal, Dr. Zhu stated that laboratory testing for plasminogen activity and antigen testing should be the next step. It will diagnose the condition. “But it could take months before a provider makes the connection [that PLGD1 is the cause].”

The extravascular, fibrin-rich lesions that appear anywhere there is mucous membranes can cause serious or even life-threatening complications. For example, the growths could cause airway obstruction, renal failure if the kidney is involved, chronic hearing loss, or blindness.

“Prior to 2023, we didn’t have an FDA-approved treatment,” she noted. Fresh frozen plasma infusions, which had low plasminogen concentrations, were the mainstay. In 2023, the FDA approved a human-derived plasminogen infusion, which effectively raises plasminogen blood concentrations and ensures adequate plasminogen activity. Plasminogen infusions must be given every two to four days. Five years after initializing therapy, patients have remained free of new lesions, said Dr. Zhu.

The adverse events associated with the infusion include infusion-site reactions, bloating, nausea, and fatigue. She also related that there is a theoretical risk for introduction of infection (as it is a blood product). The fibrin-rich growths can suddenly slough off with therapy, and this could potentially cause unique problems (e.g., a sizeable lesion in the airway breaking off) or bleeding.

0 0

Angela Zhu, MD, is an Ophthalmologist and Clinical Assistant Professor, Pediatric & Adult Cornea/Cataract/External Diseases, at Bascom Palmer Eye Institute in Miami. In this interview with
CheckRare, Dr. Zhu describes some of the key features of plasminogen deficiency and why ophthalmologists are often the healthcare providers who begin the process toward diagnosis.

Plasminogen deficiency type 1 (PLGD-1) is a rare genetic disorder in which the body fails to make adequate quantities of plasminogen, the molecule responsible for protection against abnormal fibrin clotting. It generally manifests initially (in about 80%) as ligneous conjunctivitis, in which thick membraneous lesions (from from fibrin accumulation) develop on the surface of the eye and in the eyelid. As a result, Dr. Zhu said, ophthalmologists are usually the first healthcare provider to see the patient and start the diagnostic journey.

Even though the ligneous lesions on the eye are generally the first symptom in young patients, PLGD-1 can present in many different ways (and in virtually any organ system with mucous membranes). However, fibrin accumulations in internal organs or tissue may be harder to detect.
The diagnosis may not be obvious, especially if the telltale ophthalmologic sign is misread as common infectious conjunctivitis. Patients with PLGD1 can have multiple other symptoms that wax and wane, said Dr. Zhu, and “we need to educate providers about the disease and how it can present. It is underdiagnosed and underrecognized.”

In patients with ligneous conjunctivitis, these fibrous lesions can first be mistaken for discharge, which is common in infectious conjunctivitis. But it doesn’t respond to treatment, unlike viral or bacterial causes of conjunctivitis would. Once the ligneous lesion is removed from the eye, because the plasminogen deficiency is not remedied, it will likely form again.

In the case of these eye lesions or conjunctivitis that doesn’t resolve with antiallergy, steroidal, or antiviral treatment, or grow back after removal, Dr. Zhu stated that laboratory testing for plasminogen activity and antigen testing should be the next step. It will diagnose the condition. “But it could take months before a provider makes the connection [that PLGD1 is the cause].”

The extravascular, fibrin-rich lesions that appear anywhere there is mucous membranes can cause serious or even life-threatening complications. For example, the growths could cause airway obstruction, renal failure if the kidney is involved, chronic hearing loss, or blindness.

“Prior to 2023, we didn’t have an FDA-approved treatment,” she noted. Fresh frozen plasma infusions, which had low plasminogen concentrations, were the mainstay. In 2023, the FDA approved a human-derived plasminogen infusion, which effectively raises plasminogen blood concentrations and ensures adequate plasminogen activity. Plasminogen infusions must be given every two to four days. Five years after initializing therapy, patients have remained free of new lesions, said Dr. Zhu.

The adverse events associated with the infusion include infusion-site reactions, bloating, nausea, and fatigue. She also related that there is a theoretical risk for introduction of infection (as it is a blood product). The fibrin-rich growths can suddenly slough off with therapy, and this could potentially cause unique problems (e.g., a sizeable lesion in the airway breaking off) or bleeding.

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Richard J. Auchus, MD, PhD, Professor of Internal Medicine and Pharmacology at the University of Michigan Medical School, discusses two-year results of Crenessity (crinecerfont) in the treatment of congenital adrenal hyperplasia (CAH).

CAH refers to a group of genetic conditions that affect the adrenal glands. Affected people lack an enzyme the adrenal glands need to make one or more of these hormones and often overproduce androgens. For example, females with a severe form of the condition may have ambiguous genitalia at birth and if not properly diagnosed, develop dehydration, poor feeding, diarrhea, vomiting and other health problems soon after. People with milder forms may not be diagnosed with the condition until adolescence or adulthood when they experience early signs of puberty or fertility problems.

At the 2026 American Association of Clinical Endocrinology (AACE) Annual Meeting, two-year data from the phase 3 CAHtalyst adult clinical trial of crinecerfont was presented. Crinecerfont is a potent and selective oral corticotropin-releasing factor type 1 receptor (CRF1) antagonist designed to reduce and control excess adrenocorticotropic hormone (ACTH) and adrenal androgens through a non-glucocorticoid (GC) mechanism.

The phase 3 CAHtalyst global registrational studies were designed to evaluate the safety, efficacy and tolerability of crinecerfont in children and adults with classic CAH due to 21-hydroxylase deficiency. The CAHtalyst Adult study included 182 adult patients ages 18 to 58 years. The study evaluated improvement of androgen control over four weeks of crinecerfont treatment and the enabling of GC reduction to physiologic range while androstenedione levels were maintained or improved over an additional 20 weeks of treatment.

At month 24 of the study, 69% (n=149) of participants achieved a physiologic GC dose, with many participants eliminating nonphysiologic GC types. Of participants originally taking dexamethasone (n=20), 75% switched to a dexamethasone-free regimen, while 62% (37/60) of patients taking more than two doses of hydrocortisone per day were able to eliminate a dose outright. GC dose reductions and regimen changes were achieved without worsening androstenedione levels relative to baseline, indicating that lowering the GC dose was not achieved at the expense of androgen control.

Long‑term treatment with crinecerfont was generally well tolerated, with more than 80% study retention at two years and no new safety signals observed.

Data from the CAHtalyst phase 3 studies supported approval of crinecerfont by the US Food and Drug Administration in December 2024. The open-label extension treatment portions of both studies are ongoing.  

Chronic exposure to supraphysiologic GC doses is associated with numerous long-term health risks, including cardiometabolic, bone health and quality-of-life complications. Reducing high-dose, long-term GC exposure represents one of the most important goals in the management of classic congenital adrenal hyperplasia (CAH).

To learn more about CAH and other rare endocrine disorders, visit https://checkrare.com/diseases/endocrine-disorders/

CHAPTERS
Introduction 00:00
CAH Overview 00:13
Diagnosis and Current Management 1:50
Two-Year Results 3:10
Weight and Metabolic Outcomes 4:58

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