STAR-0215 for Hereditary Angioedema
Recruiting in Palo Alto (17 mi)
+17 other locations
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2
Recruiting
Sponsor: Astria Therapeutics, Inc.
Must not be taking: ACE inhibitors, Estrogens, Androgens, others
Disqualifiers: Chronic angioedema, HAE Type III, others
No Placebo Group
Prior Safety Data
Trial Summary
What is the purpose of this trial?The goal of this trial is to enable the collection of information about long-term safety and clinical activity of STAR-0215 in participants with hereditary angioedema (HAE). Participants will receive repeat doses of STAR-0215 for up to 5 years.
Will I have to stop taking my current medications?
You may need to stop taking certain medications before joining the trial. Specifically, you should not have used angiotensin-converting enzyme inhibitors, estrogen-containing medications, or certain androgens shortly before the trial. Additionally, if you are on preventive therapies for HAE, there are specific timeframes you must follow before participating.
What data supports the effectiveness of the drug STAR-0215 (Navenibart) for hereditary angioedema?
While there is no direct data on STAR-0215 (Navenibart) for hereditary angioedema, similar treatments like donidalorsen have shown effectiveness in reducing attack frequency and improving quality of life in patients with hereditary angioedema.
12345How does the drug STAR-0215 (Navenibart) differ from other treatments for hereditary angioedema?
STAR-0215 (Navenibart) is unique because it may offer a novel mechanism of action or administration route compared to existing treatments like stanozolol, which is an androgen, and ecallantide, a protein inhibitor. While stanozolol requires careful dose management due to side effects, and ecallantide is used for acute attacks, STAR-0215 could provide a different approach, potentially with fewer side effects or a more convenient dosing schedule.
678910Eligibility Criteria
This trial is for people with hereditary angioedema who participated in a previous STAR-0215 study and met certain conditions. They shouldn't have used ACE inhibitors, estrogen medications, or androgens recently, nor should they have other chronic angioedema types or be on preventive HAE therapies without consulting the medical monitor.Inclusion Criteria
Open to participants from STAR-0215-201 (NCT05695248) who have met specific conditions related to completion of the trial or entry into the Run-In period
Discontinued STAR-0215-201 (for reasons other than safety) after having completed at least 84 days of trial follow-up since their last dose of STAR-0215 (eligibility requires consultation with the Medical Monitor)
Exclusion Criteria
I have not taken ACE inhibitors or estrogen medications in the last 28 days.
I have used specific medications for preventing HAE attacks as per the given timelines.
I have been diagnosed with a chronic form of angioedema other than hereditary.
+1 more
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Treatment
Participants receive repeat doses of STAR-0215 for up to 5 years
5 years
Every 3 months for first 2 years, every 6 months for next 3 years
Follow-up
Participants are monitored for safety and effectiveness after treatment
6 months
Participant Groups
The trial tests the long-term safety and effectiveness of repeated doses of STAR-0215 in individuals with hereditary angioedema. It's designed to last up to five years, gathering extensive data on how well this treatment works over time.
4Treatment groups
Experimental Treatment
Group I: Dose Regimen 3 (Arm D): STAR-0215Experimental Treatment1 Intervention
STAR-0215 will be administered as a subcutaneous injection.
Group II: Dose Regimen 2 (Arm B): STAR-0215Experimental Treatment1 Intervention
Participants will receive STAR-0215 every 6 months.
Group III: Dose Regimen 1 (Arm C): STAR-0215Experimental Treatment1 Intervention
STAR-0215 will be administered as a subcutaneous injection.
Group IV: Dose Regimen 1 (Arm A): STAR-0215Experimental Treatment1 Intervention
Participants will receive STAR-0215 every 3 months.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Medical Research of Arizona a Division of Allergy, Asthma & Immunology Associates, LTDScottsdale, AZ
Massachusetts General HospitalBoston, MA
Little Rock Allergy & Asthma Clinical Research CenterLittle Rock, AR
Allergy & Asthma Clinical ResearchWalnut Creek, CA
More Trial Locations
Loading ...
Who Is Running the Clinical Trial?
Astria Therapeutics, Inc.Lead Sponsor
References
Hereditary angioedema with normal C1 inhibitor in a French cohort: Clinical characteristics and response to treatment with icatibant. [2018]The clinical characteristics and icatibant-treatment outcomes of patients with hereditary angioedema with normal C1 inhibitor (HAE-nC1 INH) are limited.
Conestat alfa (ruconest): first recombinant c1 esterase inhibitor for the treatment of acute attacks in patients with hereditary angioedema. [2022]Conestat alfa (Ruconest): first recombinant C1 esterase inhibitor for the treatment of acute attacks in patients with hereditary angioedema.
A phase 2 open-label extension study of prekallikrein inhibition with donidalorsen for hereditary angioedema. [2023]Hereditary angioedema (HAE) is a potentially fatal disease characterized by unpredictable, recurrent, often disabling swelling attacks. In a randomized phase 2 study, donidalorsen reduced HAE attack frequency and improved patient quality-of-life (ISIS721744-CS2, NCT04030598). We report the 2-year interim analysis of the phase 2 open-label extension (OLE) study (ISIS 721744-CS3, NCT04307381).
Nanofiltered C1-esterase inhibitor for the acute management and prevention of hereditary angioedema attacks due to C1-inhibitor deficiency in children. [2013]To evaluate the use of Cinryze (nanofiltered C1-esterase inhibitor [C1 INH-nf]) for the acute management and prevention of hereditary angioedema attacks in the subgroup of children and adolescents who participated in 2 placebo-controlled and 2 open-label extension studies.
Hereditary angioedema with normal C1 inhibitor: clinical characteristics and treatment response with plasma-derived human C1 inhibitor concentrate (Berinert®) in a French cohort. [2017]Hereditary angioedema (HAE) is a rare genetic disorder characterised by episodes of swelling without urticaria. Berinert® (CSL Behring) is a plasma-derived human C1 inhibitor (C1-INH) concentrate, approved for the treatment of HAE with C1-INH deficiency (C1-INH-HAE), however, it is often used off-label in Europe to treat HAE with normal C1-INH. To report the clinical characteristics of patients with HAE with normal C1-INH (with F12 gene mutation; FXII-HAE) or of unknown origin (U-HAE), and their response to Berinert®. Data from 2007 to 2016 (obtained retrospectively from the French Cohort BeRinert Angiœdème [COBRA] registry of HAE patients with everyday use of Berinert®) were analysed; no control group was included. Diagnostic criteria for FXII-HAE and U-HAE included a normal C1-INH antigenic level and function and refractoriness to high-dose antihistamines. For FXII-HAE, diagnosis also included F12 gene mutation, and U-HAE a positive family history for the disease. To date, 28 patients with FXII-HAE or U-HAE were identified (mean age: 27 years; first angioedema attack at 19.8 years; 85.7% female) with 78 documented Berinert®-treated attacks, the majority occurring in the laryngeal and abdominal regions. Efficacy assessment of Berinert® was available for 38 of 78 documented Berinert®-treated attacks; 22 improved within 60 minutes of treatment initiation, nine within 60-180 minutes, four after 180 minutes, and three showed no improvement. No severe or serious adverse effects were reported. Data to date suggest that Berinert® may be a safe and efficacious treatment option for the majority of HAE patients.
Hereditary angioedema: a decade of management with stanozolol. [2019]Thirty-seven patients with hereditary angioedema, who, without therapy, had attacks of cutaneous angioedema, gastrointestinal colic, and/or upper respiratory symptoms at a frequency and severity sufficient to prompt treatment with an attenuated androgen, have been evaluated for the incidence of side effects and biochemical toxicity during various schedules leading to the minimal effective dose. Stanozolol was administered in a 2 mg daily dose, initially, and after the symptoms and signs were adequately controlled for 2 months at this dose or at 1 mg per day, the drug was administered every other day at 4 mg. Patients who responded adequately to this schedule were administered 2 or 1 mg every other day, and then the interval between doses was gradually increased to 1 week, after which the agent was stopped. Eighteen patients experienced adverse reactions to stanozolol while the minimal effective dose was attained. In each instance the side effect subsided with a reduction in dosage. The most common adverse reactions were biochemical evidence of hepatic dysfunction and, to a lesser extent, hirsutism and menstrual irregularities. Although 21 of 27 patients in an initial study of the minimal effective dose were maintained with daily therapy in 1980, by 1986 this group and 10 additional patients were distributed so that three patients were receiving daily maintenance, 18 were receiving alternate-day maintenance, and 16 patients were receiving no maintenance therapy [corrected]. Thus, stanozolol appears to be a safe and effective agent for management of hereditary angioedema when patients are continually monitored to define the minimal effective dose or the feasibility of stopping the drug.
Ecallantide: in acute hereditary angioedema. [2021]Ecallantide, a recombinant protein that is a selective, highly potent and reversible inhibitor of human plasma kallikrein, is indicated for the treatment of acute attacks of hereditary angioedema (HAE) in patients aged >or=16 years. In the randomized, double-blind, placebo-controlled, multicentre, phase III trial EDEMA3, mean symptom response to treatment at 4 hours (assessed using the Treatment Outcome Score [TOS]; primary endpoint) was significantly greater with a single subcutaneous dose of ecallantide 30 mg than with placebo in patients with acute, moderate to severe attacks of HAE. In addition, the mean change from baseline in symptom severity at 4 hours (assessed using the Mean Symptom Complex Severity [MSCS] scale) was significantly greater with ecallantide than with placebo. At 4 hours in the similarly designed EDEMA4 trial, the mean change from baseline in MSCS score (primary endpoint) and mean TOS were both significantly greater in recipients of a single subcutaneous dose of ecallantide 30 mg than in placebo recipients. Subcutaneous ecallantide 30 mg was generally well tolerated in patients with acute attacks of HAE in the EDEMA3 and EDEMA4 trials. Adverse events were mostly of mild to moderate severity, and no event that was more common in ecallantide than placebo recipients occurred in >10% of patients.
Inhibitory effects of budesonide, desloratadine and dexamethasone on cytokine release from human mast cell line (HMC-1). [2022]To determine the inhibitory potency of budesonide on interleukin (IL)-4, 6 and 8, GM-CSF and TNF-alpha release from the human mast cell line (HMC-1) in comparison with the systemic glucocorticosteroid, dexamethasone, and H(1) antagonist, desloratadine.
The Role of Combination Calcipotriol plus Betamethasone Dipropionate Gel in the Treatment of Moderate-to-Severe Scalp Seborrhoeic Dermatitis. [2022]This study aimed to investigate the off-label use of a combination calcipotriol plus betamethasone dipropionate (CBD) gel in the treatment of moderate-to-severe scalp seborrhoeic dermatitis (SSD).
Clobetasol propionate emulsion formulation foam 0.05%: review of phase II open-label and phase III randomized controlled trials in steroid-responsive dermatoses in adults and adolescents. [2013]Clobetasol propionate 0.05% emulsion foam was recently developed for use on multiple body sites.