Mitodicure GmbH applies for 3 patents for ME/CFS drugs

Here is an AI summary of Klaus Wirth's talk at a conference a couple days ago. (Starts at 5:15, language is German.)

https://www.youtube.com/watch?v=q1T_dtgBqsk

• Introduction
  • Klaus Wirth presents a comprehensive disease concept for ME/CFS
    
  • Goal: Develop an effective drug strategy as a pharmacologist and drug researcher
  • Analysis based on corona infection causing severe and complex vascular and circulatory disorder
• Circulatory Disorder and Sodium Absorption
  • Circulatory disorder leads to reduced blood flow and capillary chemical fusion
  • Muscle cells become loaded with sodium
  • Sodium-potassium ATPase transports sodium out and potassium in, requiring significant energy
  • Beta receptors may become desensitized due to high adrenaline/sympathetic nervous system activity
• Sodium Levels and Muscle Function
  • MRI studies show increased sodium in calf muscles of patients
  • Higher sodium levels correlate with worse hand strength
  • Increased intracellular sodium leads to worse action potential and excitability
  • Hand strength correlates with prognosis and symptoms
• Calcium Overload
  • High sodium levels cause sodium-calcium exchanger to reverse, importing calcium
  • Calcium overload may damage mitochondria (hypothesis)
  • Mitochondrial damage leads to less ATP production and increased oxidative stress
• Vicious Cycle and Chronicity
  • Oxidative stress further inhibits sodium pump function
  • Circulatory disorder and sodium pump dysfunction create a self-perpetuating cycle
  • Repeated damage and regeneration occur with every exertion (PEM)
  • Cumulative mitochondrial damage reinforces the vicious cycle
• Disease Progression
  • Acute infection leads to post-COVID syndrome with microvascular capillary disorder
  • Some patients (estimated 15%) develop ME/CFS
  • ME/CFS characterized as a dominant mitochondrial disorder with functional vascular damage
• Skeletal Muscle Findings
  • Clinical signs: fatigue, exhaustion, muscle weakness, pain, and cramps
  • Limited muscle strength, early onset anaerobic metabolism, reduced oxygen uptake
  • Biopsies show muscle damage and regeneration, especially after exertion
  • Biochemical and electron microscopy evidence of mitochondrial dysfunction and damage
• Proposed Treatment Approach
  • Stimulate sodium-potassium ATPase and mitochondrial sodium-calcium exchanger
  • Improve blood flow in muscles and brain
  • Reduce vascular permeability (anti-inflammatory effect)
  • Address hypervolemia and orthostatic stress
• Additional Factors
  • Renal hyperexcretion contributes to hypervolemia
  • Renin paradox: lack of expected increase in renin levels
  • Excessive production of vasoactive substances in muscles may explain various symptoms
• Drug Development
  • Active substance identified based on the proposed mechanism
  • Normal development takes about 7 years, but could potentially be shortened
  • Financing is a current challenge, causing delays in development
  • Routine work needed: safety toxicology, pharmacokinetics, etc.