Welcome to Thrombologic


Thrombologic is a clinical stage biopharmaceutical company whose focus is critical care medicine addressing life-threatening diseases that occur in severely ill patients. The first clinical indication being addressed by the company is severe community-acquired pneumonia, which has been documented as one of the most common causes of death from infection.
In these patients, inflammation has been documented to induce endothelial cell activation and platelet activation leading to lack of platelets (thrombocytopenia) and microvascular thrombus formation.  These dysfunctions lead to increased bleeding risk and immunodeficiency and are well-documented predictors of multiple organ dysfunction and death. In order to address these problems, Thrombologic has developed THR-B7 to treat and prevent thrombocytopenia and micro-thrombus formation in these patients.


An achievable treatment for the life-threatening events associated with inflammatory and infectious diseases 

Recent studies evaluating the factors associated with early death in patients with infectious diseases have reinforced the concept that in cases with systemic disease deaths are not only dependent on antibiotic efficacy but also on other factors, namely inadequate host response. In these patients, inflammation has been documented to induce endothelial cell activation and platelet activation leading to lack of platelets (thrombocytopenia) and microvascular thrombus formation.  These dysfunctions lead to increased bleeding risk and immunodeficiency and are well-documented predictors of multi-organ dysfunction and mortality. In order to address these problems, Thrombologic has developed THR-B7 to treat and prevent thrombocytopenia and micro-thrombus formation in these patients.
Emerging evidence points to the critical role of the endothelium in patients with these types of systemic infections. Endothelial activation in response to infection is associated with changes in hemostatic balance, leukocyte trafficking, vascular permeability, inflammatory response, and microcirculatory flow. Although endothelial activation evolved as an adaptive host response to infection, it can become excessive and systemically disseminated. This results in the collapse of the endothelium, causing both a leaky vascular endothelium and the endothelial cells to express receptors which enhance the hemostatic distortion, and thus, contributes to morbidity and mortality associated with systemic infections.
 
Recent data have also demonstrated a relationship between platelet count and prognosis of patients admitted to an intensive care unit (ICU) with the systemic disease, Severe Community Acquired Pneumonia. Thrombocytopenia has been shown to be a predictor of poor prognosis, whether it already existed upon ICU admission of patients or appeared during the ICU stay. It is hypothesized that thrombocytopenia results in immunodeficiency through loss of platelet-mediated immune functions and that thrombocytopenia-induced immunodeficiency in critical illness, in part, explains the negative predictive value of low or declining platelet count. The risks of thrombocytopenia not only include bleeding, but immunodeficiency and immune dysregulation as well.