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Allowing patients to hope

Vision

 Providing hope to patients suffering from chronic and degenerative diseases

 

Development Focus

Trocar Chronic and Degenerative Diseases (CDD) early-stage research program targets the development of innovative, small molecule therapeutics that mitigate chronic inflammation, fibrosis and reactive oxygen species (ROS)

Leveraging Trocar's proprietary platform technology and supported by third party, peer-reviewed scientific publications, the priority areas for Trocar CDD's early stage drug development pipeline are lung fibrosis and chronic kidney disease (CKD).

 

In addition, our COVID-19 therapeutic strategy and mechanism of action proposed in April 2020 to mitigate the cytokine storm associated with COVID-19 have also in recent months been independently validated and confirmed. 

 

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PULMONARY

FIBROSIS

Pulmonary fibrosis has high incidence, morbidity, and mortality. Current FDA approved drugs only slow the rate of progression of the disease. 

Trocar CDD is in the early stages of developing a lead candidate, small molecule for the treatment of pulmonary fibrosis that is a proven anti-fibrotic and ROS-inhibitor.

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KIDNEY DISEASE 

CKD affects 13% of Americans, and there are currently no drugs that mitigate the rapid progression of acute kidney injury (AKI) to CKD.

Trocar CDD's early stage CKD compound mechanism of action involves the activation of the RAAS* and the mitigation of excessive generation of ROS that trigger cytokine release and induction of pro-inflammatory, pro-oxidative and pro-fibrotic cytokines in AKI.

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COVID-19

In recent months, studies conducted in the US have demonstrated that statins and ARBs not only reduce the risk of developing severe COVID-19 disease but also increase patient recovery time.  

Trocar CDD has been investigating the RAAS pathway and its role in COVID-19 since early 2020 and has designed a proprietary combo pill utilizing drugs already in the clinic and developed a potential novel therapeutic agent.

Pulmonary Fibrosis
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Pulmonary fibrosis (PF) is a form of interstitial lung disease that causes scarring in the lungs. There are over 200 different types of PF and in most cases, there's no known cause. The most common type of PF is idiopathic pulmonary fibrosis (IPF). Approximately 50,000 new cases of IPF are diagnosed each year. Several identifiable diseases and conditions can lead to scarring of the lungs, but the majority of PF cases are caused by unknown reasons.

Currently, two U.S. Food and Drug Administration (FDA) approved therapies (Esbriet and OFEV) are prescribed to slow the progression of the disease. Still, IPF remains a very serious condition with patient mortality three to five years after diagnosis. 

IPF is morphologically a peripherally basilar disease of unbridled fibroblastic proliferation. Inflammation and fibrosis (scarring) occur in the walls of the alveoli and the underlying tissue. Unrelenting collagen deposition provides the foundation for progressive fibrosis leading to respiratory failure and ultimately death. 

Overproduction of reactive oxygen species (ROS) results in oxidative stress which has been demonstrated to lead to lung damage. Oxidative stress exacerbates multiple pathologic processes, including inflammation of the airways. Inflammation in turn may induce recurring DNA damage, inhibition of apoptosis, and activation of protooncogenes by initiating signal transduction pathways.

Trocar's proprietary, early stage pulmonary fibrosis compound is a conjugate of a best-in-class anti-fibrotic and a potent ROS-inhibitor. In addition, Trocar CDD has also synthesized over a dozen analogs.

Trocar CDD is partnering with George Mason on the development of its pulmonary fibrosis strategy.

 

Chronic Kidney Disease
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Chronic kidney disease (CKD) affects 13% of Americans contributing to significant morbidity and mortality. Currently, there are no drugs that mitigate the rapid progression of acute kidney injury (AKI) to chronic kidney disease (CKD). Trocar CDD’s proprietary therapeutics are designed to slow down or halt the progression of AKI to CKD and ultimately prevent end-stage renal disease (ESRD).

Although the use of angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (ARBs) represent the current standard of care for CKD patients with proteinuria, patients progressively lose kidney function while on these medications. Moreover, most patients with CKD never reach ESRD because they die prematurely most frequently from cardiovascular disease (CVD). Therefore, therapies to prevent or slow the progression of CKD would be highly significant and fill a major unmet medical need.
 

It is becoming increasingly recognized that activation of the renin angiotensin aldosterone system (RAAS) and excessive generation of reactive oxygen species (ROS) trigger cytokine release and induction of pro-inflammatory, pro-oxidative and pro-fibrotic cytokines in AKI. This RAAS and ROS mediated activation is caused by hyper-induction of angiotensin II (Ang II) that binds to the AT1 receptor found on epithelial and endothelial cells in many tissues (e.g. lung, cardiovascular and kidney).

The mechanisms of action for Trocar’s CKD, tissue-targeted technologies involve the RAAS and ROS signaling via the AT1 receptor. The Trocar Pharma team has generated patented compounds that upregulate ACE2 and reduce intracellular ROS. Trocar CDD's novel drugs are catalytic antioxidants linked to FDA approved drugs that increase the angiotensin converting enzyme 2 (ACE2). These therapeutics provide superior anti-oxidant, anti-inflammatory, anti-fibrotic vascular and renoprotective effects. This double anti-oxidant approach has the expected added advantage of triggering re-activation of the cytoprotective ACE2 receptor. Third-party validation studies report that ACE2 administration slows kidney damage by reducing the activity of RAAS and counteracting its adverse effects by converting Ang II into angiotensin 1-7.

 

Trocar's new CKD therapies are designed to quench ROS and boost the epithelial and endothelial cytoprotective ACE2 dependent mechanisms that ultimately prevent progression of renal disease.

Trocar CDD is partnering with the University of Oklahoma on the development of its CKD therapeutic strategy.

 
 
COVID-19
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Trocar Pharma's hypothesis is that a novel, clinically validated therapeutic agent that disrupts the infective machinery of SARS-CoV-2 virus (severe acute respiratory syndrome coronavirus 2), on cells in the lung, gastrointestinal (GI) tract and heart, would have a major impact on the devastating COVID-19 pandemic.

Our hypothesis is based on observations that the angiotensin converting enzyme 2 (ACE2) is the binding site for SARS-CoV-2, the virus implicated in the current COVID-19 pandemic. This receptor is the same site of entry for the current SARS-CoV-2 virus and the renin angiotensin system (RAS) is highly activated during SARS-CoV-2 infection. 

Trocar Pharma’s COVID-19 therapeutics are structured to mitigate the harmful effects of COVID-19 by mediating the host’s response and restoring the cell’s natural homeostasis. Trocar Pharma’s COVID-19 therapeutics would be the first agent to restore the cell’s response to COVID-19 infection, expecting to result in improved survival and reduced toxicity.

​Trocar CDD has been investigating the RAAS pathway and its role in COVID-19 since March 2020 and has developed both a proprietary combo pill utilizing drugs already in the clinic and a novel therapeutic agent.

Trocar CDD is collaborating with George Mason University and the University of Oklahoma on the development of its COVID-19 therapeutics.