Bioprovar Corporation

An Innovative Immune Therapy With Antibiotics to Treat Deadly Excess Inflammation in Sepsis and Ards Induced From Severe Bacterial Infection in Geriatric Patients - There Are 1,665,000 Cases of Sepsis Annually in the U.s. (H-CUP#122) With Near 500,000 Associated Deaths, and Currently, No Fda Approved Treatment. Ards (acute Respiratory Distress Syndrome) and Sepsis Are Medical Emergencies Requiring Intensive Care and Are Fatal in 30-70% of Cases. Ards and Sepsis Are Main Causes of Death in Geriatric Patients. They Develop Severe Infection From Bacteria Producing Deadly Toxins. Enterobacteriaceae, Pseudomonas Aeruginosa, Salmonella SPP, and Staphylococcus Aureus Are Largely at Cause. These Toxins Drive the Immune Response to a Deadly Excess. They Bind to Platelets (PT), Activating Them to Express a Ligand for TREM1 (triggering Receptor Expressed on Myeloid Cells 1), a Potent Activation Receptor of Macrophages (MF) and Neutrophils. Multiple Activated PT Ligands Bind to MF, Overtrigger TREM1, Hyperactivating MF to Release Large Amounts of Inflammatory Mediators Producing an Excess of Systemic Inflammatory Response (sir). Active MF Expressing TREM1 Are Characteristic of Sepsis and Ards. Over 450 Scientific Articles Document the Role of TREM1 in Inflammation. Bioprovar's Scientists Have Discovered TREM1-SV, a Natural Splice Variant Competitive Receptor of TREM1 Found in the Blood and Regulating the TREM1-ACTIVATION Pathway (tap). as an Immune Therapy With Antibiotics (at), TREM1-SV Showed a Strong Efficacy to Increase Survival Probability in Mice With Sir From Cecum-ligation Puncture (CLP), Improving Survival From 0% (at Alone) to 67%. Per Comparison, Inhibiting the Lps-activation Pathway With a Peptide Blocking the Toll-like Receptor 4 Had No Significant Effect on Survival. Based on These Data and Current Knowledge, Bioprovar Is Developing Biotremvartm to Administer Supplement of Human Recombinant (hu R) TREM1-SV With Antibiotics to Sepsis and Ards Patients to Alleviate Sir and Prevent Death. the Rationale Is That by Competing for the Excess of TREM1 Ligands, TREM1-SV Regulates Tap by Reducing the Number of TREM1-LIGAND Complexes That Trigger Activation, Thwarting MF Hyperactivation, Hence Maintaining an Effective Immune Response. Our Objective Here Is to Gather the Preclinical Data Needed for the Ind-enabling Work of GLP Production and Toxicology Studies. We Aim to Optimize Non-glp Production of Hu RTREM1-SV With a System Transferable to CGMP and Perform Analytical Characterization of Its Structural Identity. Biotremvar's Broad Therapeutic Efficacy Will Be Demonstrated as an Immune Therapy With Antibiotics in Animal Models of Clp-induced Sir Using Different Doses and Regimens. Using a Mouse and a Guinea Pig (nonrodent) Animal Model, We Will Generate Pharmacodynamic, Pharmacokinetic, PK/PD Relationship Data, and Calculate the Half-life of Biotremvartm. Bioprovar Owns the Rights to TREM1-SV. Our Long-term Goal Is to Validate Biotremvartm CGMP in Solution for Intravenous Injection to Treat Sepsis and Ards Patients. It Is Vital to Have a Therapeutic Broadly Effective at Suppressing the Central Mechanism Sustaining These Diseases. the Use of Biotremvartm to Inhibit Sir in Sepsis or Ards Is Innovative, Scientifically Grounded, and Will Save Many Lives.