TB-500 and GHK-Cu are in milligrams
A bunch of mitochondrial proteins have succinylation modification, such as UCP1 in thermogenic function, GLUD1 in glutamate metabolism, SDH in ETC, the TCA cycle, GLS2 and CPS1 in glutaminolysis, ECHA and VLCAD in FAO, HMGCS2 in ketogenesis and SHMT2 in serine catabolism
Heres how they work together: Folates role: Dietary folate converts to 5-MTHF (active folate) via the MTHFR enzyme 5-MTHF donates a methyl group to homocysteine This requires B12 as a cofactor for the enzyme methionine synthase The result: homocysteine converts to methionine B12s role: B12 (as methylcobalamin) acts as a cofactor for methionine synthase It helps transfer the methyl group from 5-MTHF to homocysteine Without adequate B12, folate gets trapped and cant donate its methyl group This is called the methyl trap What happens when one is deficient: Low B12 with adequate folate: Folate cant function properly (methyl trap) Homocysteine rises despite good folate levels Methylation slows down Can mask B12 deficiency symptoms initially Low folate with adequate B12: Not enough methyl groups available for donation Homocysteine rises Methylation impaired DNA synthesis affected Both low: Severe methylation impairment Very high homocysteine Anemia (megaloblastic) Neurological damage risk Why MTHFR mutations affect this partnership: With MTHFR mutations: Your body cant efficiently convert folate to 5-MTHF This creates a bottleneck in the methylation cycle Even with adequate B12, you dont have enough active folate to work with it Result: elevated homocysteine, poor methylation The solution: Bypass the MTHFR bottleneck by taking pre-methylated folate (5-MTHF) that doesnt require conversion
Nie, czenie eksperymentalnych peptydw bez nadzoru medycznego drastycznie zwiksza ryzyko skutkw ubocznych i powanych reakcji immunologicznych
Representative data of four experiments (n = 3)
With that in mind its expected to submit the drug for regulatory approval towards the end of 2025, meaning it may be available as soon as 2026
