View clinical trials related to Covid19.
Filter by:The disease caused by the new coronavirus, SARS-CoV-2, called COVID-19, it has considered a worldwide pandemia by the WHO. Suddently, it produces a lot of patients severe ill, in a little geographic area, that could surpase the resourses of the any health system in the world. There is no documentation of an effective alternative for the treatment of the severe ill patients, that can reduce the mortality or the adverse events suffered by these people. It is has suggested the usefulness of the Mesenchymal Stem cells (MSC) for the management of these patients, thanks to their direct and indirect antiviral capacity, and its potency as immunomodulator, that could ameliorate the lung disease and the severity of COVID-19.
This is a phase 2 multi-center, double-blind, randomized, placebo-control clinical trial with 200 subjects who have never been infected by COVID-19 (SARS-Cov-2 virus screen test negative, no blood SARS-Cov-2 IgM and IgG antibodies detected during enrollment) followed by a pilot study of 5 subjects to demonstrate the safety of proposed three-dose regimen of autologous AdMSCs infusions. The 100 study subjects who have previously banked their AdMSCs with Celltex, will receive three doses of autologous AdMSCs (approximately 200 million cells) intravenous infusion every three days. The 100 subjects in the control group who have previously banked their AdMSCs with Celltex will not receive any Celltex's AdMSC therapy but placebo treatments. All subjects are monitored for safety (adverse events/severe adverse events), COVID-19 symptoms, SARS-Cov-2 virus test, blood SARS-Cov-2 IgM and IgG antibodies tests, blood cytokine and inflammatory (CRP, IL_6, IL-10, TNFα) tests and disease severity evaluation for 6 months after the last dose of AdMSC infusion for the study group and 6 months after the enrollment for the control group.
GC004 is a Phase I trial to evaluate the safety and the immune responses of a therapeutic vaccine in SARS-CoV-2 infected patients. Covid-19 confirmed patients with mild or no symptoms will be enrolled sequentially into low dose and high dose groups. Following the vaccination subjects who received at least one vaccination will be followed for safety through week 26.
Resident cells of human adipose tissue express ACE2 and DPP4, receptors for SARS-Cov2. The hypothesis is that the virus may enter and spread in fat depots.
COVID 19, which probably started from zoonotic transmission related to crowded markets in China was announced as a pandemic by the WHO on 11 March 2020. There is currently no clinically proven specific antiviral agents available for SARS-CoV-2 infection. Supportive treatment, including oxygen therapy, fluid management, and broad-spectrum antibiotics to cover secondary bacterial infection, remains the most important management strategy. Since its discovery, lactoferrin and its related peptides are considered non-specific host defense molecules against a broad range of viruses including SARS-CoV, which is closely related to SARS-CoV-2 that causes COVID-19. Besides reducing viral entry, lactoferrin can also suppress virus replication after the viral entry and has an immunomodulatory effect that can prevent the cytokine storm associated with COVID-19. The aim of our study is to assess the safety and efficacy of lactoferrin within the context of SARS-CoV-2 and propose the possibility of supplemental lactoferrin as a potential preventive drug for healthcare workers exposed to SARS-CoV-2.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected the global population with significant morbidity and mortality. One of the main concerns is the management of the patients since there is no specific treatment for this condition. Therefore, in SARS-CoV-2 patients the compassionate use of off-label therapies has been initiated; such as the use of plasma from convalescent patients. This treatment has been used in other pandemics like SARS-CoV-1, H5N1, H1N1, Ebola, among others. This study is a phase II/III randomized clinical trial to assess the effectiveness and safety of convalescent plasma administration in patients with high-risk SARS-CoV-2.
To evaluate the efficacy and safety of azvudine in treatment of COVID-19
This is a multi-center, randomized, double-blind, placebo-controlled, phase III clinical study to evaluate the efficacy of Favipiravir combined with supportive care for adult patients with COVID-19-Moderate type.
Living in Canada and being health-worker in the first line face to COVID-19, investigator outcome is to teach an experience or explain the disease using a review and get people prepared to COVID-19 treatment focused on adherence to the HIV approved 2006-2007 protocol at Ghent University but the review shows an older different study approved at the University of Kinshasa and its ethics approval that again is an old document. So no ethics document supporting the study exists as it is now and no registration. It is an observational study and therefore would not usually require registration in order for the results to be published. It is not a type of secondary literature. The formula TOMEKA® (Mix porridge of maize, sorghum, and soya) follows FOOD + HEALTH CLAIM. It is scientifically justified, relevantly used, and correctly communicated. Methodology: sufficient data? scientific consensus? correct methodology? correct population? context: significant results? context of use, realistic ingestion? correct target group? communication: consumer perception? exaggerated/insinuative, clear, precise, complete, correct information? not misleading? correctly presented? The product TOMEKA® tried to fulfill to above questions in a fitting way with COVID-19 which is an emerging, rapidly evolving situation without a vaccine.
COVID19-associated disease may have different clinical aspects classified in 3 stages. Some patients initially presenting with a non-hypoxemic viral pneumonia (stage 2a) may evolve toward a more severe stage 2b or 3 (acute respiratory distress syndrome, ARDS) around the 7th or 10th day of evolution, with a severe biological inflammatory syndrome (CRP>200 mg/l), and some times more severe complications such as acute renal insufficiency, consumptive coagulopathy or shock, requiring increasing oxygen therapy, ICU admission, invasive mechanical ventilation and possibly leading to death. This detrimental evolution is due to a host-derived "cytokine storm" with a great excess of circulating inflammatory cytokines. In animal models of ARDS complicating coronavirus or influenza virus infection, the cytokine storm has been linked to hyperactivation of the NLRP3 inflammasome. NLRP3 constitutes an intracellular protein platform which is responsible for caspase1 activation and processing of interleukin (IL)-1beta and IL-18 . IL-1b is a major proinflammatory cytokine which induces IL-6, whereas IL-18 is an inducer of interferon gamma (IFNg) production by Th-1 lymphocytes. A blood IL-1/IL-6 signature can be defined by increased neutrophilia and CRP concentrations, whereas an IL-18/IFNg signature is characterized by severe hyperferritinemia, consumptive coagulopathy and cytopenia. A majority of patients with COVID-19 infections seems to have an IL-1/IL-6 signature, evolving in the more severe forms toward an IL-18/IFNg signature, mimicking cytokine profiles observed in other inflammatory diseases such as Still's disease or hemophagocytic syndromes. In Still's disease, therapeutic inhibition of IL-1 or IL-6 has proven to be very efficient strategies. During hemophagocytic syndromes, inhibition of IFNg is effective in humans notably through blockade of its receptor signalization, using the JAK kinase inhibitor ruxolitinib. Following this strategy, we propose to use biological drugs currently available for inhibition of IL-1 (anakinra), IL-6 (tocilizumab) or IFNg signaling (ruxolitinib) in the severe forms of COVID19-associated disease. Our hypothesis is that IL-1, IL-6 or JAK kinase inhibition will allow: 1. to prevent stage 2b worsening and the need to be admitted in ICU, by decreasing oxygen-requirement and systemic inflammation 2. to improve stage 3 and extremely severe stage 3, allowing invasive mechanical ventilation weaning, improving multi-system organ dysfunction, leading to a faster ICU exit. We propose an open randomized therapeutic trial (1/1/1) on 216 patients with severe stage 2b and 3 of the disease