Sachlichkeit
Iron
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- May 11, 2025
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1. GH IGF-1 Axis. HGH is still the most effective drug for growing. Note; HGH doesn't actually make you grow, IGF-1 which is a downstream of HGH does.
2. Testosterone directly upregulates IGF-1 expression in muscle and bone growth. Estrogen closes growth plates
3. CNP C type natriuretic peptide. CNP is the signal to tell your bones to keep growing at the growth plate. It also inhibits FGFR3 which tells your growth plates to stop growing. CNP ANALOGS are drugs that stimulate CNP.
The only two clinically approved are VOSORITIDE and TransConCNP. Too expensive. There are also cheaper drugs such as Infigratinib that inhibit FGFR3 without stimulating CNP. dwarfism is caused by overactive FGFR3, under-regulating it in normal people could theoretically yield an increase in height but it wont be as effective as upregulating CNP.
4. WNT beta catenin. CNP tells bones to grow is a sort of authoritative signal, WNT actively follows its instructions. It wakes up inactive stem cells and converts them into bone building cells (osteoblasts). It multiplies the cartilage cells that stack on top of each other and ossify into solid bone (chrondrocytes). over-upregulation of WNT closes plates early by accelerating choondrocyte maturity. Your growth plates ossify from cartilage to bone faster, but because of how fast your cells are aging you now have an imbalance between young chondrocytes (cartilage) and old chondrocytes (bone) so growth stops.
WNT activators are: CHIR99021, Used to increase WNT in animal testing. 38% increase of WNT in human cells. There are no human studies. This is a lab chemical intended for research. KY19382. Well established offlabel use. Topical application for hair growth, sometimes injected by biohackers for accelerated repair. KY is non water soluble, its hard to dissolve. In animal studies it is dissolved in DMSO and mixed with .9 sterile saline for injection at a rate of 1:10-1:9. Lithium, resveratrol, and Andrographolide are supplements that upregulate WNT. Anything WNT related should be cycled instead of taken every day to mitigate the risk of closing growth plates early. If you can find some drug that slows chondrocyte maturation you can reap the benefits of increased WNT while mitigating the side effect of early closure.
5. TGF BETA inhibition. TGF BETA regulates growth. TGF beta too high, production of chondrocytes is slowed down and they stay immature. (They don't ossify from cartilage into bone.) Mice with overactive TGF beta had 30-40% shorter limbs. CONTROLLED INHIBITION of TGF beta makes your limbs longer and thicker. total inhibition of tgf beta unregulates growth you are going to get cancer and abnormal bone formations and stuff. So either cycle high dose TGF inhibitors with rest periods in between or use a moderate inhibitor for longterm use. Best is Fresolimumab (experimental.) Then pirfenidone, used to treat fibrosis, Losartan, blood pressure medication, and andrographolide which is a supplement. The rest are research chemicals.
6. PTH ANALOGS. Post puberty bone growth. Popularized for frame increase but still relevant for height. Used to treat people at risk of bone fracture (osteoporosis.) slows down chondrocyte maturity, prevents growth plate closure by maintaining the zone of the growth plate where chondrocytes multiply, increases localized IGF-1 production, and regulates the genes responsible for chondrocyte fate. (Sox9 and Runx2.) These genes determine what cells become chondrocytes. Cells can decide to either become an osteoblast and build bone (density and width) or become a chondrocyte and contribute to vertical growth.
Chronic activation of PTH breaks bone down. Short term pulses builds bone. If your plates are closed, PTH will still stimulate osteoblasts + chondrocytes but you will only increase in width because your growth plates are fused.
Drugs are Abolaparatide and Teriparatide. PTH-134 is the offlabel lyophilized version of Teriparatide. Both of these drugs have a half life of one hour so the risk of chronic activation is very low. Abolaparatide is better than PTH-134. Lower risk, more measured increase in bone growth. When reconstituted both drugs decay at room temperature in 24 hours so you have to buy them in lyophilized form and reconstitute them. Store in freezer at -20C, if you are using PTH-134 thaw a vial in the fridge every 7-14 days. If you are using abolaparatide its once a month. Both last a max of 3 months reconstituted when frozen.
MECHANICAL LOADING. Physical exercise. Avoid squats, deadlifts, etc. Will increase bone density at the cost of reducing longitudinal growth. Weighted stretching, jumping, sprinting, swimming, cycling. Add forms of resistance to stimulate growth. You will get more growth out of your bones running around with a backpack full of bricks compared to running without one
There are more pathways but I've been led to believe they are largely irrelevant so just focused on the main ones.
TLDR?
2. Testosterone directly upregulates IGF-1 expression in muscle and bone growth. Estrogen closes growth plates
3. CNP C type natriuretic peptide. CNP is the signal to tell your bones to keep growing at the growth plate. It also inhibits FGFR3 which tells your growth plates to stop growing. CNP ANALOGS are drugs that stimulate CNP.
The only two clinically approved are VOSORITIDE and TransConCNP. Too expensive. There are also cheaper drugs such as Infigratinib that inhibit FGFR3 without stimulating CNP. dwarfism is caused by overactive FGFR3, under-regulating it in normal people could theoretically yield an increase in height but it wont be as effective as upregulating CNP.
4. WNT beta catenin. CNP tells bones to grow is a sort of authoritative signal, WNT actively follows its instructions. It wakes up inactive stem cells and converts them into bone building cells (osteoblasts). It multiplies the cartilage cells that stack on top of each other and ossify into solid bone (chrondrocytes). over-upregulation of WNT closes plates early by accelerating choondrocyte maturity. Your growth plates ossify from cartilage to bone faster, but because of how fast your cells are aging you now have an imbalance between young chondrocytes (cartilage) and old chondrocytes (bone) so growth stops.
WNT activators are: CHIR99021, Used to increase WNT in animal testing. 38% increase of WNT in human cells. There are no human studies. This is a lab chemical intended for research. KY19382. Well established offlabel use. Topical application for hair growth, sometimes injected by biohackers for accelerated repair. KY is non water soluble, its hard to dissolve. In animal studies it is dissolved in DMSO and mixed with .9 sterile saline for injection at a rate of 1:10-1:9. Lithium, resveratrol, and Andrographolide are supplements that upregulate WNT. Anything WNT related should be cycled instead of taken every day to mitigate the risk of closing growth plates early. If you can find some drug that slows chondrocyte maturation you can reap the benefits of increased WNT while mitigating the side effect of early closure.
5. TGF BETA inhibition. TGF BETA regulates growth. TGF beta too high, production of chondrocytes is slowed down and they stay immature. (They don't ossify from cartilage into bone.) Mice with overactive TGF beta had 30-40% shorter limbs. CONTROLLED INHIBITION of TGF beta makes your limbs longer and thicker. total inhibition of tgf beta unregulates growth you are going to get cancer and abnormal bone formations and stuff. So either cycle high dose TGF inhibitors with rest periods in between or use a moderate inhibitor for longterm use. Best is Fresolimumab (experimental.) Then pirfenidone, used to treat fibrosis, Losartan, blood pressure medication, and andrographolide which is a supplement. The rest are research chemicals.
6. PTH ANALOGS. Post puberty bone growth. Popularized for frame increase but still relevant for height. Used to treat people at risk of bone fracture (osteoporosis.) slows down chondrocyte maturity, prevents growth plate closure by maintaining the zone of the growth plate where chondrocytes multiply, increases localized IGF-1 production, and regulates the genes responsible for chondrocyte fate. (Sox9 and Runx2.) These genes determine what cells become chondrocytes. Cells can decide to either become an osteoblast and build bone (density and width) or become a chondrocyte and contribute to vertical growth.
Chronic activation of PTH breaks bone down. Short term pulses builds bone. If your plates are closed, PTH will still stimulate osteoblasts + chondrocytes but you will only increase in width because your growth plates are fused.
Drugs are Abolaparatide and Teriparatide. PTH-134 is the offlabel lyophilized version of Teriparatide. Both of these drugs have a half life of one hour so the risk of chronic activation is very low. Abolaparatide is better than PTH-134. Lower risk, more measured increase in bone growth. When reconstituted both drugs decay at room temperature in 24 hours so you have to buy them in lyophilized form and reconstitute them. Store in freezer at -20C, if you are using PTH-134 thaw a vial in the fridge every 7-14 days. If you are using abolaparatide its once a month. Both last a max of 3 months reconstituted when frozen.
MECHANICAL LOADING. Physical exercise. Avoid squats, deadlifts, etc. Will increase bone density at the cost of reducing longitudinal growth. Weighted stretching, jumping, sprinting, swimming, cycling. Add forms of resistance to stimulate growth. You will get more growth out of your bones running around with a backpack full of bricks compared to running without one
There are more pathways but I've been led to believe they are largely irrelevant so just focused on the main ones.
TLDR?
