The diseases targeted by EHP involve multiple pathophysiological processes throughout the body. Existing drugs currently focus on some of these processes, but don’t address the critical multi-factorial nature of these diseases, leading to the significant unmet medical needs existing today.
Systemic sclerosis (SSc) is an autoimmune disease that causes inflammation and then fibrosis of skin, blood vessels and internal organs that progressively decreases quality of life, leading to death in the majority of cases. There are no specific therapeutics approved for systemic sclerosis. Current treatments target the inflammatory component of the disease, providing some symptomatic relief, but none alter disease progression. To achieve a notable impact for the patient, it is important to also prevent fibrosis and vascular damage. Based on its MOA, our product candidate for systemic sclerosis has the potential to slow, stop, or reverse disease progression.
The hallmark of multiple sclerosis (MS) is demyelination, which is the breakdown of the protective myelin sheath surrounding nerves that aids in conducting nerve impulses. This breakdown is initiated by autoimmune processes that cause inflammation. Current therapeutics are primarily anti-inflammatory or immunosuppressive. They provide some symptomatic benefits, but have troublesome side effects. To achieve a notable impact on patients’ quality of life and the potential for disease modification, we need an intervention that affects the early stages of the disease so that inflammation is reduced, autoimmunity is addressed (without the toxicities of immunosuppression) and demyelination is slowed or stopped).
Our product candidate for multiple sclerosis affects the key physiological targets in the body that influence the underlying cause to slow, stop, or even reverse the progression of the disease while causing minimal side effects.
The four hallmarks of Parkinson’s disease (PD) are tremors (shaking) of the hands, arms, legs and face; stiffness; bradykinesia (slow movement); and difficulty with balance and coordination. The main drug development strategy to date focuses primarily on the dopaminergic system, which provides only partial, mostly symptomatic temporary treatment. So far, the drugs tried and tested for neuroprotection have failed.
Current treatments address mainly motor symptoms but not non-motor symptoms, which often start earlier and are overall more detrimental to patient well-being and quality of life. Holistic approaches with multiple modes of action are needed with new treatments rather than using single target approaches such as those only affecting the dopaminergic system.
Huntington’s disease (HD) is a rare neurodegenerative genetic disorder. This chronic, complex disease is characterized by a triad of symptoms, including motor impairment, decline in cognitive function, and psychiatric disturbances. Current medications can lessen some symptoms, such as drugs that help control movement, and antidepressants and antipsychotics for psychiatric issues, but no treatments can alter the course of the disease. To make a notable impact for the patient, it is important to optimize patients’ quality of life by addressing symptoms and maximizing their ability to live and function independently for as long as possible while also providing the potential to affect the progression of the disease.