A wellness and youthification drug, and longevity drug could be producible at when Adenosine, the amino acid, at a new drug form where the adenosine is linked to a membrane transport molecule or protein, could possibly increase the amount of adenosine triphosphate that gets made because there is more substrate adenosine at the cytoplasm to enhance with PO4 groups. One possibility is chlorophenoxy adenosine, the chlorophenoxy group gets it past membranes, then it is available adenosine at cytes; I perceive I read that lipophilic molecules have better trasnport past the blood brain barrier, so as those are cytomembranes that get passed, it is possible that a lipophilic variation of adensine could be an ATP heightening supplement. You might just be able to put a /\/\/\/\/\ alkane tail on the adenosine, possibly detachable and at the same molecular location the PO4 attaches to at ATP; it is possible an adenosine-O-/\/\/\/\/\ where an oxygen links to the alkane would still be lipophilic enough to pass the cytomemebrane while the oxygen linker makes it easy for the cyte to metabolize into available adenosine (and the “extra” lipophilic alkane part); another possible cytomembrane passing adenosine molecule is a branched phosphoalkane (like a phosphorus clover, but with methyls or ethyls instead of Os at a PO4 shape).

At adensosine/\/\/\, I do not know how big that alkane has to be to be lipophilic, it is possible, besides an alkane, or branched very mulimethyly alkane, that a lipophilic keytone could provide enough lipophilicity to get the adenosine past the cytomembrane while being harmless when the ATP supplement is converted to adenosine (and thus ATP) as well as the extra molecule parts that are at the cytosol, at doses that imaginably 100 mg to grams a day of supplement. If there are any ketones that are good for people, then those might be beneficial moeities for the adenosine. The other thing I have perceived is that butyls are sort of harmless or beneficial, I have vague memories of circulating butryate being beneficial soperhaps the adenosine/\/\/\/\ could be a butyl, or a branched butyl.

The thing to make a cytosol ATP-available amount increasing supplement with depends on if the phosphorylator reaction chemicals are replete with lots of PO4, and could use more adenosine. If alternatively, they could use more PO4, then PO4 linked to a membrane transport chemical, like something lipophilic, or a peptide or protein could bring PO4 to the cyte, heightening the amount of PO4 available for cycling and recycling at the ADP->ATP cytoprocess; another approach would be to increase P phosphorus recycling at the body, at the cyte and cytoplasm, it is possible there is some sort of phophorous export channel that a drug could downregulate, or possibly heightening the amount of, or upregulating an enzyme that turns phosphorus containing proteins that get recycled or other phosphorus containing stuff, so that there is more available phosphorus to make PO4 from. Another actual amount of ATP at the cytological ADP->ATP available chemical pool raising drug or supplement could be a drug that caused people to only pee out 1/4 to 1/2 as much phosphorus then this could be measured as to if it increased the amount of functioning ATP, or if mice meaured throughout their lives have longer healthspan and greater lifespan from having more ATP, longer, than other mice.

I read 90 lbs of ADP gets turned into ATP each 24 hours, so it is possible that the thing that affects the amount of ATP available at the cyte and cytoplasm is actually the amount of adenosine, as the phosphorylation looks highly available at 90 pounds every 24 hours.

Longevity genes and drugs: different cytes hve different numbers of mitochondria, do existing SNPs of well humans cause different higher amounts of mitochondria at particulr cytotypes. Imaginably leukocytes have 200 mitochondria each, but hepatocytes have 700. Are there naturally occuring genes or SNPs (single nucleotide polymoprhisms) that cause a leukocyte to have 700 mitochondria or a then noting that at those gene variants or SNPs, that a 60% decline of mitochondria number across the lifespan just moves a leukocyte to 200 from 320 mitochondria per cyte, or a hepatocyte to 700 from 1120 mitochondria, or any kind of body cyte or tissue’s mitochondria to the average of that of a gentically pre-optimized person.

Photoactive chemotherapy is described at published literature, and lithotripsy of solid objects at the body is published. It is possible that the double slit/binomat local area bandpass energy or also chemical filter could have local tissue applications as well.

I should think of a pill that cures cancer at the developing world, like a tissue localized chemotherapeutic with really minimal side effects, or a precancer senolytic like chemical that only concentrates at cytes that are precanecrous.

Similarly, it is possible that loading up the cytoplasm with alpha-helice (or better) constructed bandpass binomats, which unless they bioconcentrate in some way automatically (they might, or could be engineerable to custom concentrate kind of like mitochondria or also membranes concentrate chemical colors); If the bandpass binomats do not bioconcentrate then even as diffuse molecules they might have some engineerable effect as cytoplasm thickeners, “modelling with percolation theory new cytoplasm chemicals” which might then also be new drugs

If increasing or decreasing the fluidity of the cytoplasm 20-40% causes some beneficial effect then along with binomat drugs as well as drugs that have effects modellable with percolation theory, are producible. Increasing or decreasing the fluidity of the cytoplasm can also be accomplished with gene therapy. Looking at the wellness and lonvevity of people with differing cytoplasmic fluidity or also cyte as gel-bag stands up from viscosity morphology, and osmotic profile measurables produces data that can be used to find indications of use, and effects of new fluidity/viscosity/osmotics drugs..

As a beauty drug,
lyse a radiolabelled cyte, then put the goop outside the cytomembrane of a well dermatocyte, then find out which specific chemicals at cytoplasm are able to migrate into a cyte. It is possible some of those chemicals, which can be taken up adermatocyte from topical application, are easy and simple to produce. These new membrane-passing fluidity/viscosity/osmological chemicals are topically active things that cause the gel-bag perspective firmness of hydrated skin, and with the gel-bag perspective of cytomorphology have the same gel-bag standupness, whihc possibly causes youthful morphology like youthful skin.

GSK, online content So, find out what at just released cytoplasm will pass the cytomembrane of a well cyte, then make a big list of those chemicals, any of theose chemicals that do something could be new drugs that easily pass the cytomembrane, also new molecular variants on those cytomembrane passing naturally occuring chemicals could be new drugs. Even cytochemicals without an obvious drug effect like cytoplasm thickeners (imaginably NaPCA like proteins) could be used as tissue firming, youthful morphology producing ingredients that are actually absorbed and utilized from topical application..

and possibly also cause the dermatocytes to be bnearer their younger shape, that is morphology.

The production of hyalonuric acid and collagen at dermatocytes is, I perceive, chemicals actually at the cytoplasm of dermatocytes changing stiffness, osmological things, and cytoplasms gelness, conriuting to well tissue. So cytoplasm thickeners and thinners measured as to their longevity and wellness effects could be beneficial new drugs. biological systems where viscosity of cytoplasm has beneficial aspects like dermis exist, so optimizing that viscosity, osmologicalness, and morphology effecting gel-bag function could be a new kind of beneficial drugs.

Actin/tubulin amplifiers, possibly (deuterated actin might be a gradualized motion track, modified actin protein, possibly even a new SNP could make fast travel actin, each of the fast and gradual versions could be measured as to effect on wellness and longevity.

GSK, drug localization and Math: If there is an effect with the double slit stripes being taller than the laser dot, while being narrower, there might be some kind of math or physics relation where if you measure one well, the other measurement beceomes less efffective (atom electron position or velocity as measurable thing), or if there is another, different photonic system where: “if it thinks it can’t go littler it can still make x and y directions different sizes, but equationally resolved to be ok, such that one math/physics funtional measurable, like height, is much larger than another measurable like width” That causes the technology opportunity of making a beam system where if you cannot tell how tall it is, it gets to be arbitrarily skinny? Just thinking if this is a known supported math or physics phenomena, where one characteristic of a thing observable at a high resolution makes the other less observable so the system observability amount remains constant (kind of reminded of position and velocity at atoms and electrons); the idea is that you then take one of these “high resolution at one spatial axis if you skip measuring the rest” math or physics equation relationship function effects, and then build a localization beam out of it, so that way as compared with a laser dot, a cofocalization, or even a venn diagram overlap, you can make a crosshairs, sort of like one double slit “|||||||||” output layered on another “=“ to produce really optimized as tiny areas to localize the beam effect with. So that double slit crosshairs (or similar better approach) is a way to make acoustically activateable drugs, or also photonically activateable drugs have even higher addressible spatial resolution at human tissue.