NoNO-42 for Stroke
Recruiting in Palo Alto (17 mi)
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2
Recruiting
Sponsor: NoNO Inc.
Disqualifiers: Pregnancy, Severe illness, others
Prior Safety Data
Trial Summary
What is the purpose of this trial?ACT-42 is a domain of the ACT-GLOBAL platform (NCT06352632).
This trial is a Phase 2b, multicenter, prospective, randomized, open label, blinded-endpoint (PROBE) controlled single-dose adaptive trial.
A total of up to 600 male and female participants aged ≥ 45 to ≤ 90 years harboring an acute ischemic stroke who are eligible for an intravenous thrombolytic with or without endovascular thrombectomy therapy will be enrolled within 3 hours of stroke onset/last known well.
Will I have to stop taking my current medications?
The trial information does not specify whether you need to stop taking your current medications. It's best to discuss this with the trial coordinators or your doctor.
What safety data exists for NoNO-42 or similar treatments in humans?
There is limited safety information available for NXY-059, a similar treatment, which has been studied in combination with another stroke treatment. The study looked at effects on bleeding and brain damage, as well as blood sugar and body temperature, but detailed safety results are not provided.
12345How does the drug NoNO-42 for stroke differ from other treatments?
NoNO-42 is unique because it may involve components like Notoginsenoside R1, which promotes brain recovery by encouraging new brain cell growth through specific pathways (BDNF/Akt/CREB). This is different from other treatments like nitric oxide donors, which focus on improving blood flow and reducing blood pressure shortly after a stroke.
678910Eligibility Criteria
This trial is for men and women aged 45 to 90 who've had a stroke recently (within the last 3 hours) and are eligible for clot-busting treatment or a procedure to remove the clot. They should have a moderate-to-severe stroke, be able to live independently before the stroke, and give informed consent.Inclusion Criteria
I am chosen for clot-dissolving treatment for my stroke.
I was enrolled in the study within 3 hours of my symptoms starting.
I am between 45 and 90 years old.
+4 more
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
3 hours
Treatment
Participants receive a single, 20-minute intravenous dose of NoNO-42 or placebo
20 minutes
1 visit (in-person)
Follow-up
Participants are monitored for safety and effectiveness after treatment
90 days
Multiple contacts over 90 days
Participant Groups
The NoNO-42 Trial tests whether a single dose of NoNO-42 can help people recovering from an acute ischemic stroke better than a placebo. Participants will either receive this new drug or a placebo alongside standard treatments like thrombolysis or thrombectomy.
2Treatment groups
Active Control
Placebo Group
Group I: NoNO-42Active Control1 Intervention
Randomized participants will be given a single, 2.6 mg/kg 20-minute intravenous dose of NoNO-42 with a target start time of less than 10 minutes from randomization.
Group II: PlaceboPlacebo Group1 Intervention
Randomized participants will be given a single 20-minute intravenous dose of placebo (comprising normal saline infusion only) with a target start time of less than 10 minutes from randomization.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
University of Calgary - Foothills Medical CentreCalgary, Canada
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Who Is Running the Clinical Trial?
NoNO Inc.Lead Sponsor
References
Online Tool to Improve Stratification of Adverse Events in Stroke Clinical Trials. [2021]Knowing characteristic adverse events (AEs) and their incidence among patients participating in acute stroke trials may assist interpretation of future studies. We aimed to develop an online tool to inform stroke trial safety.
Neurologic safety event rates in the SENTIS trial control population. [2013]Adverse event (AE) rates for interventional stroke trials are not well established.
Characteristic adverse events and their incidence among patients participating in acute ischemic stroke trials. [2022]Adverse events (AE) in trial populations present a major burden to researchers and patients, yet most events are unrelated to investigational treatment. We aimed to develop a coherent list of expected AEs, whose incidence can be predicted by patient characteristics that will inform future trials and perhaps general poststroke care.
Use of cilostazol for secondary stroke prevention: an old dog with new tricks? [2018]To evaluate the safety and efficacy of cilostazol for secondary prevention of non-cardioembolic ischemic stroke.
Effects of the spin trap agent disodium- [tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (generic NXY-059) on intracerebral hemorrhage in a rabbit Large clot embolic stroke model: combination studies with tissue plasminogen activator. [2019]It has been proposed that the novel spin trap agent disodium-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) may be useful in the treatment of ischemia and stroke. To date, there is little information concerning the safety of NXY-059 when administered in combination with the only Food and Drug Administration-approved pharmacological agent for the treatment of stroke, the thrombolytic tissue plasminogen activator (tPA). Thus, we determined the effects of NXY-059G, a generic form of NXY-059, on hemorrhage and infarct rate and volume when administered alone or in combination with tPA. In addition, we determined whether NXY-059G affected 2 physiological variables, blood glucose levels and body temperature.
A systematic review of nitric oxide donors and L-arginine in experimental stroke; effects on infarct size and cerebral blood flow. [2022]Nitric oxide (NO) is a candidate treatment for acute ischaemic stroke, however published studies in experimental stroke have given conflicting results.
[Protective effect of notoginsenoside R1 on neuron injury induced by OGD/R through ATF6/Akt signaling pathway]. [2018]Notoginsenoside R1(NGR1),a critical compound in traditional herb Panax notoginseng, is a kind of estrogen receptor agonist.It is reported to exhibit anti-apoptotic,anti-oxidative and anti-inflammatory properties activity, so it is widely used for treatment of various diseases.In order to investigate the potential neuroprotective effect of NGR1 in hypoxic-ischemic brain damage(HIBD), primary cortical neurons were used in this study to establish oxygen-glucose deprivation/reoxygenation(OGD/R) injury models. They were treated with NGR1 and estrogen receptor inhibitor ICI-182780 respectively, then the neuronal survival, cell membrane integrity and apoptosis were assessed by MTT assay,lactate dehydrogenase test(LDH) and Hoechst 33342 stain respectively, while the protein expression levels of ATF6α,p-Akt,Akt,Bax and Cleaved Caspase-3 were measured by Western blotting. Results indicated that as compared with the blank control group,OGD/R could induce cell injury and apoptosis(P
Notoginsenoside R1 Improves Cerebral Ischemia/Reperfusion Injury by Promoting Neurogenesis via the BDNF/Akt/CREB Pathway. [2021]Notoginsenoside R1 (R1), a major component isolated from P. notoginseng, is a phytoestrogen that exerts many neuroprotective effects in a rat model of ischemic stroke. However, its long-term effects on neurogenesis and neurological restoration after ischemic stroke have not been investigated. The aim of this study was to evaluate the effects of R1 on neurogenesis and long-term functional recovery after ischemic stroke. We used male Sprague-Dawley rats subjected to middle cerebral artery occlusion/reperfusion (MCAO/R). R1 was administered by intraperitoneal (i.p.) injection immediately postischemia. We showed that R1 significantly decreased infarct volume and neuronal loss, restored neurological function, and stimulated neurogenesis and oligodendrogenesis in rats subjected to MCAO/R. More importantly, R1 promoted neuronal proliferation in PC12 cells in vitro. The proneurogenic effects of R1 were associated with the activation of Akt/cAMP responsive element-binding protein, as shown by the R1-induced increase in brain-derived neurotrophic factor (BDNF) expression, and with the activation of neurological function, which was partially eliminated by selective inhibitors of BDNF and PI3K. We demonstrated that R1 is a promising compound that exerts neuroprotective and proneurogenic effects, possibly via the activation of BDNF/Akt/CREB signaling. These findings offer insight into exploring new mechanisms in long-term functional recovery after R1 treatment of ischemic stroke.
Effect of Treatment Delay, Stroke Type, and Thrombolysis on the Effect of Glyceryl Trinitrate, a Nitric Oxide Donor, on Outcome after Acute Stroke: A Systematic Review and Meta-Analysis of Individual Patient from Randomised Trials. [2022]Background. Nitric oxide (NO) donors are a candidate treatment for acute stroke and two trials have suggested that they might improve outcome if administered within 4-6 hours of stroke onset. We assessed the safety and efficacy of NO donors using individual patient data (IPD) from completed trials. Methods. Randomised controlled trials of NO donors in patients with acute or subacute stroke were identified and IPD sought from the trialists. The effect of NO donor versus control on functional outcome was assessed using the modified Rankin scale (mRS) and death, by time to randomisation. Secondary outcomes included measures of disability, mood, and quality of life. Results. Five trials (4,197 participants) were identified, all involving glyceryl trinitrate (GTN). Compared with control, GTN lowered blood pressure by 7.4/3.3 mmHg. At day 90, GTN did not alter any clinical measures. However, in 312 patients randomised within 6 hours of stroke onset, GTN was associated with beneficial shifts in the mRS (odds ratio (OR) 0.52, 95% confidence interval (CI) 0.34-0.78) and reduced death (OR 0.32, 95% CI 0.14-0.78). Conclusions. NO donors do not alter outcome in patients with recent stroke. However, when administered within 6 hours, NO donors might improve outcomes in both ischaemic and haemorrhagic stroke.
The role of nitric oxide in stroke. [2022]Stroke is considered to be an acute cerebrovascular disease, including ischemic stroke and hemorrhagic stroke. The high incidence and poor prognosis of stroke suggest that it is a highly disabling and highly lethal disease which can pose a serious threat to human health. Nitric oxide (NO), a common gas in nature, which is often thought as a toxic gas, because of its intimate relationship with the pathological processes of many diseases, especially in the regulation of blood flow and cell inflammation. However, recent years have witnessed an increased interest that NO plays a significant and positive role in stroke as an essential gas signal molecule. In view of the fact that the neuroprotective effect of NO is closely related to its concentration, cell type and time, only in the appropriate circumstances can NO play a protective effect. The purpose of this review is to summarize the roles of NO in ischemic stroke and hemorrhagic stroke.