MCTR1 for COVID-19

c19early.org

COVID-19 Treatment Clinical Evidence

COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets. c19early analyzes 6,000+ studies for 210+ treatments—over 17 million hours of research. Only three high-profit early treatments are approved in the US. In reality, many treatments reduce risk, with 25 low-cost treatments approved across 163 countries.

Naso/oropharyngeal treatment Effective Treatment directly to the primary source of initial infection.
Healthy lifestyles Protective Exercise, sunlight, a healthy diet, and good sleep all reduce risk.
Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
Acetaminophen Harmful Increased risk of severe outcomes and mortality.
Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.

MCTR1 may be beneficial for COVID-19 according to the studies below. COVID-19 involves the interplay of 400+ viral and host proteins and factors providing many therapeutic targets. Scientists have proposed 11,000+ potential treatments. c19early.org analyzes 210+ treatments. We have not reviewed MCTR1 in detail.

Studies suggesting benefit with MCTR1

Ma et al., Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies, Signal Transduction and Targeted Therapy, doi:10.1038/s41392-025-02127-9

Abstract In recent years, the incidence of acute respiratory distress syndrome (ARDS) has been gradually increasing. Despite advances in supportive care, ARDS remains a significant cause of morbidity and mortality in critically ill patients. ARDS is characterized by acute hypoxaemic respiratory failure with diffuse pulmonary inflammation and bilateral edema due to excessive alveolocapillary permeability in patients with non-cardiogenic pulmonary diseases. Over the past seven decades, our understanding of the pathology and clinical characteristics of ARDS has evolved significantly, yet it remains an area of active research and discovery. ARDS is highly heterogeneous, including diverse pathological causes, clinical presentations, and treatment responses, presenting a significant challenge for clinicians and researchers. In this review, we comprehensively discuss the latest advancements in ARDS research, focusing on its heterogeneity, pathophysiological mechanisms, and emerging therapeutic approaches, such as cellular therapy, immunotherapy, and targeted therapy. Moreover, we also examine the pathological characteristics of COVID-19-related ARDS and discuss the corresponding therapeutic approaches. In the face of challenges posed by ARDS heterogeneity, recent advancements offer hope for improved patient outcomes. Further research is essential to translate these findings into effective clinical interventions and personalized treatment approaches for ARDS, ultimately leading to better outcomes for patients suffering from ARDS.

Huang et al., Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS), Respiratory Research, doi:10.1186/s12931-024-02678-5

AbstractAcute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities with refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With the outbreak of coronavirus disease 19 worldwide, the mortality of ARDS has increased correspondingly. Comprehending the pathophysiology and the underlying molecular mechanisms of ARDS may thus be essential to developing effective therapeutic strategies and reducing mortality. To facilitate further understanding of its pathogenesis and exploring novel therapeutics, this review provides comprehensive information of ARDS from pathophysiology to molecular mechanisms and presents targeted therapeutics. We first describe the pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress. Next, we summarize the molecular mechanisms and signaling pathways related to the above four aspects of ARDS pathophysiology, along with the latest research progress. Finally, we discuss the emerging therapeutic strategies that show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies and mesenchymal stromal cell therapies, highlighting the pathophysiological basis and the influences on signal transduction pathways for their use.