ARKAY Therapeutics, LogoFollow Us:LinkedIn
Phone Icon (609) 362-6818

About Us

Type 2 diabetes is a chronic inflammatory disease. It is characterized by the elevated fasting glucose levels, impaired glucose tolerance and impairment of the first and the second phase  of insulin secretion which occur due to inflammation-mediated progressive deterioration of pancreatic beta cell function. Impairment of beta-cell function compromises their inherent capacity to compensate for insulin resistance. Pro-inflammatory signals originating from the activation of immune dysregulation, Renin-Angiotensin System (RAS) and Cyclooxygenase-2 (COX-2) contribute to progressive reduction in the beta-cell mass and consequential state of insulin dependency. Functional response of beta cells and insulin sensitivity of insulin-responsive tissues such as liver and skeletal muscle are tightly regulated by a feed-back loop. This feedback loop determines the normal regulation of glucose metabolism by adjusting the glucagon-insulin molar ratio. There is direct correlation between magnitude of beta cells response and sensitivity of insulin-responsive tissues to insulin. As tissues develop insulin resistance, beta cells compensate with an increased output of insulin. Blood glucose levels rise in the presence of insulin resistance when beta cells are incapable of releasing sufficient insulin due to progressive deterioration of beta cell function. If pro-inflammatory signals are not blocked with the right combination of drugs, there will be progressive reduction in pancreatic beta cell mass due to inflammation-triggered apoptosis which leads to an irreversible state of pancreatic beta cell failure, a stage at which Type 2 diabetes becomes indistinguishable from Type 1 diabetes. The only treatment option available to patients at that stage is insulin therapy.  

In spite of intense mono- and combination therapies with the existing modalities, there's a progressive deterioration of metabolic control of glucose homeostasis which is indicative of progressive deterioration of beta cell function. ARKAY is committed to filling clinically the most important gap that currently exists in the modalities used for the treatment of Type 2 diabetes by targeting multiple distinct and overlapping mechanisms along the immune dysregulation-inflammation-insulin resistance axis that contribute to beta cell dysfunction. The complex etiology of Type 2 diabetes involves impairment of function of a variety of cell types that contribute to deterioration of beta cell function which triggers insulin resistance. ARKAY is advancing an innovative and novel anti-inflammatory 'Beta-cell-centric' platform that treats beta-cell dysfunction and maintains its inherent capacity to compensate for insulin resistance.

Recently, Dr. Stan Schwartz, one of ARKAY's scientific advisors described the 'Egregious Eleven' pathways and defects that contribute to hyperglycemia in his 'Beta-cell-centric' construct with beta-cell damage as the FINAL COMMON DENOMINATOR (Diabetes Care 2016; 39:179-186). To provide long-term sustainable glycemic control, the ideal therapeutic option has to favorably modulate maximum number of the 'Egregious Eleven' pathways with a minimum number of orally-active active drugs that are safe for chronic use in the early stages of progressive deterioration of beta-cell function soon after a patient is diagnosed for Prediabetes or Type 2 diabetes when pancreas still contains a restorable critical mass of beta cells. RK-01 favorably modulates either directly or indirectly ten out of the eleven of these pathways which we anticipate would contribute to long-term sustainable glycemic control, prevent or delay initiation of insulin therapy as well as prevent, delay or reduce the severity of diabetes-related complications. ARKAY's scientific rationale and the product concept is supported further by the consensus opinion of experts of the ADA, AACE, EASD and JDRF which highlighted the importance of targeting inflammation-mediated beta-cell destruction, progressive deterioration of beta-cell function and emphasized their role in the natural history of the pathophysiology of diabetes in an article that was published recently (Skyler, J.S. et al. 2017; Diabetes 66: 241-255). We are on track to bring our novel and innovative orally-active 'Beta-cell centric' combination product, RK-01 to the market by 2020. 

Major Pathophysiologic Defects in Type 2 Diabetes
Beta Cell Destruction

Personalized Medicines for Metabolic Syndrome

Even in the age of advanced medicine, Insulin Resistance Syndrome, or Metabolic Syndrome, continues to be an unmet medical need. The "one-size-fits-all" approach has failed to provide sustainable overall clinical benefit to Type 2 diabetes patients. This is due to the complex pathophysiology of the disease, as it contributes to a unique pathophysiological phenomenon in each individual patient.

Backed by 30 years of experience in this area of medicine, ARKAY Therapeutics has developed scientific, clinical, and formulation strategies to fill the gap that exists in Type 2 diabetes treatment options. By achieving therapeutic and kinetic synergies, we are on track to develop personalized medicines for patients who are stratified for lacking adequate therapeutic efficacy and overall clinical benefit with current mono- and combination therapies.


ParamAushadam

ParamAushadamTM

Derived from Sanskrit, it means "Perfect Medicine" in English.

A pharmaceutical finished product methods and formulations technology platform that
combines therapeutically efficacious doses of drugs with predetermined modified drug release kinetics to achieve optimal therapeutic as well as kinetic synergies by sparing adverse side effects as well as eliminating potential drug-drug interactions.

"Synergistically improved pharmaceutical made from a combination of pharmaceuticals for use in the treatment of diabetes; synergistically improved pharmaceutical made from a combination of pharmaceuticals for the treatment of obesity-triggered diseases, namely, diabetes and breast cancer; synergistically improved pharmaceutical made from a combination of pharmaceuticals for the treatment of conditions that coexist with diabetes, namely, non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD), arthritis and polycystic ovarian syndrome (PCOS); synergistically improved pharmaceutical made from a combination of pharmaceuticals for the treatment of diabetes-related complications, namely, nephropathy, retinopathy, neuropathy, stroke and skin ulcers"


Product Timeline

What Sets Us Apart

RK-01 is mechanistically and clinically different from currently marketed drugs.  It is an innovative and novel 'Beta-cell centric' combination product. RK-01 fills clinically the most important gap that exists in the modlaities used for the drugs on the market. Currently, there are no pancreatic 'beta-cell centric' products on the market. RK-01 will be custom formulated to provide sustainable glycemic control by maintaining or restoring beta-cell function.  FDC (Fixed Dose Combination) tablets or capsules will also reduce the pill burden and achieve better efficacy, safety, and patient compliance.

If you are interested in investing in our biopharmaceutical company, click here. For any general questions on our operations, reach us at (609) 362-6818.


New Advancements in Treatment of Type 2 Diabetes

Metabolic disease is an inflammatory disease. Based on preclinical and clinical data, anti-inflammatory 'Beta cell-centric' therapy represents a new shift in the paradigm of clinically managing optimal glycemic control efficiently, particularly in obese patients with Type 2 diabetes.

Paving New Roads in Diabetes Treatment

Our New Therapeutic Entities (NTEs) are expected to treat patient-specific comorbidities as well as the underlying cause of the complex pathophysiology of diabetes.  More importantly, they are anticipated to prevent, delay or reduce the severity of diabetes-related complications.