Embotricin™ is the first ever, non-toxic, anti-thromboembolic oral drug proven to prevent and reverse arterial plaques in animal testing. Embotricin™ effectively and specifically protects, repairs and prevents damage to the arterial lining which is now widely recognized as a therapeutic and diagnostic target for vascular disease – the endothelial glycocalyx.  In addition Embotricin™ also reduces inflammation and oxidation.     

Therapeutic Development

Embotricin™ is a novel, first in class atherosclerosis therapy with unique mechanisms of action. Whereas an infectious disease is caused by a single agent and typically respond to a single drug (antibiotic); a chronic disease including CVD is multifactorial and therefore a correspondingly multi-component drug is needed for effective treatment leading to curative outcomes.


The etiology of CVD starts with disruption of the blood vessel lining, particularly the endothelial glycocalyx, followed by oxidative damage and a cascade of inflammation, creating osmotic imbalance resulting in plaques and atherosclerosis. Embotricin™ is a triple combo drug that addresses the multifactorial causes of CVD; it is the first ever anti-thromboembolic drug proven to be effective in preventing and eliminating plaque formation in our proprietary (mice) animal model against CVD.  Moreover, it is an oral, non-toxic drug with a safety index of 20X the effective dose.


The triple drug combo is a novel approach to drug development. We synthesized 8 novel drugs, which can be franchised in the development of curative drugs against other chronic diseases including diabetes, metabolic syndrome, arthritis, cancer, and neurodegenerative diseases.

Structures of 9 proprietary FTX compounds synthesized for specific targets


Animal Model Development

The knockout ApoE mice (apoE*3-Leiden, apoE−/−) are the standard model for atherosclerosis but do not represent clinical settings:  

  • no studies yet showing plaques that become disrupted spontaneously. 

  • fatal human plaques are fibrous lesions without necrotic cores.                          

  • No appropriate animal model available                                                                                                                          


Most importantly, there is no animal model that represents glycocalyx disruption in relation to CVD.  Incidental rat models have been used to assess glycocalyx disruption (shedding of syndecan-1 and heparan sulfate) in hyperglycemia, inflammation and ischaemia-reperfusion injury and coagulation function after hemorrhagic shock.


To evaluate drug leads, Dr. J.B. Tunac developed a mouse model that mimics CVD and the thromboembolic cascade (information and data available upon patent filing). This involves feeding mice with high fat diet and exposure to biological and chemical agents, which resulted in a mouse that produced well-formed subendothelial plaques.

Drug Evaluation

The complex nature of thromboembolism does not lend to a one-drug treatment. Thus, our proprietary approach was not to administer compounds as monotherapies, but as combo drugs formulated as one pill. The traditional drug development paradigm is one drug-one disease. Thus, in an abbreviated factorial design, we rationally formulated drug combinations (3-drug combos) and tested them in the animal model.

Study Results

Drug treatment with Embotricin™ removed the plaque as evidenced by the prevention or restoration of glycocalyx components including hyaluronan (HAS-1), heparan SO4 (HS), and syndecan-1 (SDC-1)

Also, Embotricin™ was both curative and preventive of clot formation as evidenced by the marker plasminogen activator inhibitor -1 (PAI-1), which corroborates clinical data.

Based on these experimental observations, the proposed mode of action of Embotricin™ includes restoration of the glycocalyx (FTX-214), anti-oxidant (FTX-218), and antiinflammatory (FTX-219) activities.

FTX 214, 218, 219 were well tolerated when administered up to a dose of 200 mg/kg. Adverse effects were observed only at the 1000 mg/kg dose (3,000 mg/kg in combination) with one animal dying and the other five showing lethargy immediately after dosing, thus the maximal tolerated dose is up to 1000 mg/kg for each compound when administered in combination by a single oral gavage.

Dosing Toxicology

Embotricin   Highlights

(a) Consists of three components, formulated as one pill and administered orally.

(b) The effective human dose of each component (Based on animal trials) is 50 mg. and toxicological testing has shown that the maximum tolerated dose (MTD) is at least 750 mg/kg which is 15X greater than the effective dosage.

(c) The first anti-thromboembolic drug to address the root cause of the family of CV Diseases and particularly Coronary Heart Disease, a breakthrough therapy with a medical impact equivalent to penicillin.


(d) Repairs the endothelial glycocalyx, the newly recognized lining of the vascular endothelium, which when disrupted starts cardiovascular diseases (CVD), of which coronary heart disease (CHD) is the most common.

(e) First in class pill that targets thromboembolism (clotting or thrombosis), which is the ultimate cause of death.

(f) Both prophylactic and therapeutic activity.


(g) Pre-clinical animal testing demonstrated safety and efficacy.


(h) Direct replacement for and eliminates the need for statin therapies in ~90% of patient population.


(I) Embotricin™ is the first ever, non-toxic anti-thromboembolic pill proven to prevent and reverse arterial plaques in animal testing.


(j) Embotricin™ effectively and specifically protects, repairs and prevents damage to the arterial lining which is known to be the root cause of the family of cardiovascular diseases – the Endothelial Glycocalyx. 


(k) Embotricin™ prevents endothelial glycocalyx disruption as well as arterial oxidation and inflammation.     

Our intellectual properties include;

Drug Treatment and Biomarker Panel Targeted to Diseases Due to Multifactorial Ontology of Glycocalyx Disruption.

Biomarkers of Vascular Disease.

Methods and Compositions for Reversing Disruption of the Glycocalyx, Inflammation and Oxidative Damage.

(Draft) Animal Model for CVD and Inflammation.

Innovation Meets High Impact and Unmet Need

7 panel GDF (GlycocardiaGEN) – Clinical Data

Blood levels of 7 detritus components were obtained from published literature of patients with coronary heart disease (CHD), heart failure (HF), and hypertension and a virtual fingerprint was constructed. Each disease showed a unique fingerprint, which confirms the effectiveness of the GDF technology as a unique tool for identifying and monitoring treatments for diseases.

Introducing the Glycalyx Detritus Fingerprint   (GDF)

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