Raw J-147 powder (1146963-51-0) hplc≥98% | AASraw SARMS powder

     

Raw J-147 powder (1146963-51-0) hplc≥98% | AASraw SARMS powder

J-147 powder

I.Raw J-147 powder basic Characters:

Name: J-147 powder
CAS: 1146963-51-0
Molecular Formula: C18H17F3N2O2
Molecular Weight: 350.3349896
Melt Point: 177-178°C
Storage Temp: 4°C
Color: White or off white powder

II. Raw J-147 powder in enhance brain function and an extra boost cycle

1. Names:
J-147 powder

2.Raw J-147 powder Usage:
Using a drug discovery scheme for Alzheimer’s disease (AD) that is based upon multiple pathologies of old age, we identified a potent compound with efficacy in rodent memory and AD animal models. Since this compound, J147, is a phenyl hydrazide, there was concern that it can be metabolized to aromatic amines/hydrazines that are potentially carcinogenic. To explore this possibility, we examined the metabolites of J147 in human and mouse microsomes and mouse plasma. It is shown that J147 is not metabolized to aromatic amines or hydrazines, that the scaffold is exceptionally stable, and that the oxidative metabolites are also neuroprotective. It is concluded that the major metabolites of J147 may contribute to its biological activity in animals.
J-147 powder, derived from the curry spice component curcumin, has low toxicity and actually reverses damage in neurons associated with Alzheimer’s.

J147 was the mitochondrial protein known as ATP synthase, specifically ATP5A, a subunit of that protein. ATP synthase is involved in the mitochondrial generation of ATP, which cells use for energy.

The researchers demonstrated that by reducing the activity of ATP synthase, they were able to protect neuronal cells from a number of toxicities associated with the aging of the brain. One reason for this neuroprotective effect is thought to be the role of excitotoxicity in neuronal cell damage.

Excitotoxicity is the pathological process by which neurons are damaged and killed by the overactivation of receptors for the excitatory neurotransmitter glutamate. Think of it being a bit like a light switch being turned on and off so rapidly that it ends up causing the light bulb to blow.

Recently, the role of ATP synthase inhibition for neuroprotection against excitotoxic damage was demonstrated in a mouse study[4]. The second study showed that mouse models expressing the human form of mutant ATPase inhibitory factor 1 (hIF1), which causes a sustained inhibition of ATP synthase, were more resilient to neuronal death after excitotoxic damage. This data is consistent with this new J147 study, in which an increase in IF1 in the mice reduced the activity of ATP synthase (specifically ATP5A) and was neuroprotective.

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