Introduction:
Heightmaxing is not a single method, but a combination of targeting multiple biological pathways that regulate growth. This includes both stimulating mechanism that promote height, and minimizing or delaying the factors that limit it. (Do remember that genetics play a big role in this)
The goal is to shift the body into a more growth-favorable state. Supporting process like growth signaling, while attempting to reduce constraints such as premature growth plate senescence and hormonal limitations. This is extremely important because we are living in a highly hormonal disruptive environment.
While some factors are fixed, others may be influenced to a degree. Understanding where intervention is possible and where it is not is the key to approaching this in a safer, efficient and more structured way.
Do understand that while some of these have been proven anecdotally and in the medical field, a chunk of it is theoretical framework based on known mechanisms, not everything is guaranteed.
Before you also get into the rest of the guide. You can already tell this is high effort. It is high effort for a reason. You're messing with growth pathways, with things even acting as growth limiter inhibitors. There is a risk of cancer.
Section 1: GH Axis
I was going to say...
All heightmaxing stacks start with HGH.
Growth hormone lowers certain breaks that are negative for height, while also working positively for height. While many people claim diminishing returns at 6-8iu daily, this is EXTREMELY irrelevant. We want quite literally as much as we can afford. It is so irrelevant that there is actually a rule associated with this. The rule of gear and especially GH is as high as you can tolerate and as much as you can afford.
There is also a specific study, can't find it right now but will link it later down the line. But summed up..
There was mice with no GH receptors (which also means they had no IGF-1) grew 60% less, while the mice with only no IGF-1 grew 33% less. Proving that GH is just as important as IGF-1.
8iu minimum, ideally you would go way higher. You will pin this 3 hours after eating, and 1-2 hours later eat a meal with carbs and protein, then you will go to sleep.
Here is an example timeline:
5pm: Eat meal --> 8pm: Pin --> 9-10pm: Eat carb and protein meal ---> Sleep
Just to reiterate for you
8iu MINIMUM
5pm: eat
8pm: pin
9-10pm: eat carb and protein
Then sleep.
GHRP’s
GHRPs, what are they?
GHRP stands for Growth Hormone Releasing Peptide. A synthetic peptide made to have your body release growth hormone by activating the ghrelin receptor. Some people know this as the growth hormone secretagogue receptor, or for short GHSR-1a.
What does this mean?
Well first of all, it is a GH releasing peptide, so it will release more GH along side the natural pulses your pituitary gland makes. The way this works is with the ghrelin receptor, what that also means is that you will be extremely hungry. Some GHRPs are stronger, some are weaker.
The oldest GHRP made, and its pretty well known. It's most well known for causing a very strong increase in appetite, with many people becoming noticeably hungrier within 15–30 minutes of taking it, making it popular for bulking or for those who struggle to eat enough. It also releases a pretty strong amount of GH. The most common side effects are intense hunger, a temporary feeling of warmth or flushing, and mild increases in prolactin and cortisol in some people.
A stronger version of GHRP-6, but not when it comes to appetite, but the strength of GH release it does is stronger than GHRP-6. Basically GHRP-6 with a stronger GH release and less appetite. This is ideal for GH release while GHRP-6 is ideal for more of an appetite.
Considered one of the most potent GHRPs. Producing larger growth hormone pulses than GHRP-2, GHRP-6, or Ipamorelin in many studies. Unlike GHRP-6, it usually causes little to no increase in appetite, making it a popular option for those who want stronger GH release without feeling constantly hungry. Same sides as before except desensitization of the ghrelin receptor with prolonged continuous use.
Like the other GHRPs, it increases natural GH pulses rather than supplying growth hormone directly, but it is known for being much more selective, causing little to no increase in prolactin, cortisol, or appetite at typical doses. The most common side effects are mild and may include temporary warmth or flushing, with significantly fewer hormonal side effects compared to GHRP-2, GHRP-6, or Hexarelin.
Pick either one, I personally would say GHRP would be better applicable in a theoretical heigh focused setting because of the receptor desensitization from Hexarelin.
GHRP-2: 500mcg split morning/night (250mcg morning and night)
Hexarelin: 200mcg split morning/night
GHRH’s
Growth Hormone-Releasing Hormone (GHRH) are peptides that increase growth hormone release by activating the GHRH receptor on the pituitary gland. Unlike GHRPs, which stimulate the ghrelin receptor, GHRH analogs work through the body's normal growth hormone signaling pathway, encouraging the pituitary to release its own natural GH. Their biggest advantage is that they produce natural, physiological pulses of growth hormone while preserving the body's normal feedback mechanisms, making their release pattern more similar to how GH is produced naturally.
One of first widely used GHRH analogs and shortest fully active fragment of GHRH. It makes a brief but solid GH pulse that closely matches natural physiology. But due to its very short half life, it's not ideal for growth.
First of all before I explain what No DAC or DAC is, I will explain what CJC-1295 is. CJC-1295 is a modified version of Sermorelin, it contains amino acid substitutions that significantly improve resistance to enzymatic breakdown. This results in a stronger, longer and more sustainable GH pulse.
Now what is DAC and what's the difference? DAC is basically like an ester, or if you know more about insulin then it is how fast/long acting it is. DAC stands for Drug Affinity Complex, which when attached to a peptide (such as CJC-1295) it allows it to bind to serum albumin and remain active for around one week. So what does this mean?
CJC No DAC = Upgraded sermorelin, in longer and stronger pulses.
Ex: turning on and off a faucet immediately
CJC With DAC = Upgraded Sermorelin, stronger but not in pulses, lasts a week.
Ex: letting a faucet drip over time
One of the most clinically backed GHRH analogs. It is a stabilized derivative that also maintains pulsatile secretion. Basically getting a 2 in 1.
CJC No DAC: 300mcg split morning and night
GHS-1RAs
Now, this is the one people know a lot about mainly because of one compound in there. I haven't mentioned it at all so far, so you can probably guess what it is. But before that lets explain GHS a bit.
GHS-R1a Agonists - compounds that activate Growth Hormone Secretagogue Receptor (GHS-R1a), commonly known as the ghrelin receptor. This receptor is one of the primary pathways the body uses to increase growth hormone output.
Now, you already know GHRHs activates the GHRH receptor but GHS-R1a agonists work by stimulating the ghrelin receptor while also reducing the effects of somatostatin, a hormone that normally suppresses growth hormone release. This dual mechanism produces larger, more powerful GH pulses, making them some of the strongest stimulators of your body's natural growth hormone production.
There is 2 different option, but I won't even list the other one just because of how strongly the other option mogs.
And you guys have been thinking it the whole time. Insulin resistance speedrun, severe hunger in a pill, HGH levels of sleep. You know exactly what I am talking about.
MK-677 is one of the most well known, if not, THE most well known secretagogue. Popular for it being a non injectable, non peptide GHS-R1a agonist. It is orally active, doesn't cause liver stress and remains active for around 24 hours.
This makes MK-677 one of the easiest options for increases your body's GH levels since it is extremely easily sourced, not injectable, can be in a liquid solution or a pill, and it is a easy once a day dosing.
(obviously) MK-677: 15-50mg daily, before bed or morning, either one is fine (dose is dependent on full GH axis stack)
Synergy
HGH → Provides a steady baseline of circulating GH
GHRH analog → Stimulates the pituitary through the GHRH receptor
GHRP → Amplifies pituitary GH release via the ghrelin receptor and reduced somatostatin activity
GHSR-1a agonist → Further activates the ghrelin pathway
So imagine all of that together.
Ideal GH axis would be this (itll be relisted theoretical stack):
HGH
GHRP-2/Ipamorelin
CJC No Dac
MK-677
Section 2: Estrogen/E2
This is one of the most controversial ones people talk about when it comes to height. Mainly because people claim there is a very large amount of draw backs (and I agree, there is.) of Letrozole 2.5mg. It is taken right after injecting Testosterone, or Aromasin 12.5mg, ideally 25mg every day taken right after injecting Testosterone on an empty stomach.
We want to make sure that our e2 is LOW.
Now since you read that you will be making claims about brain development.
Your brain actually never stops developing and has a multitude of catchup mechanisms if it occurs. It occurs if brain development is disrupted. But you don't need to worry about that because these compounds do not have the effect on the brain that you think they do.
If you ARE worried about missing brain development, you can take Arimidex instead, there is an enzyme that transports it out of the brain, resulting in the lowest blood concentration to brain concentration of an AI, so you can have higher localized e2 with aromasin.
So best is Letrozole or Arimidex. Pick your poison.
There are a bunch of common misconceptions and not fully correct thought process that people also have. It will be mentioned and explained below.
First of all, exorbitant doses (this will be talked about in the Testosterone section) are not ideal at all.
Bone resorption only occurs in negligible parts of growth and health.
Lowers IGF-1, yes it does. But not by a lot. Around the average of 50ng.
Now in turn, this is what you get.
MONTHS of extra growth.
Less limits.
Mental and mood benefits.
(You will be depressed to hell if ran without test)
Estrogen has been damaging your plates. Yes it has. And it has been damaging them for YEARS.
It doesn't matter if you have 100 E2 or 0 E2 because in the end your plates will close (obviously 0 E2 is better, just trying to prove a point). You plates WILL close in the end, this is a process we can not reverse. Another process you can't reverse, or at least fully, is the plate damage it has done, if we could reverse it fully then we would all be 9ft Chads but that's not happening... because our cells already knows estrogen exists, so it will get detected and issues arise.
But for every problem, there is a solution. Or at least a treatment.
It will be listed later in the module.
Serms
A SERM is a Selective Estrogen Receptor Modulator. What it does is it binds to estrogen receptors and blocks estrogen's effects in certain tissues, while acting differently in others. This one will be split into two since I have two things I want to talk about. Let's get into it.
Endoxifen - the main active metabolite of tamoxifen. Tamoxifen has to be converted into endoxifen by the liver enzyme CYP2D6, so having endoxifen itself will bypass this issue because some people have genetic variants that make CYP2D6 work poorly, so they produce much less endoxifen and may receive less benefit from tamoxifen.
Tamoxifen - also known as the brand the Nolvadex. Same situation as Endoxifen. Tamoxifen converts into Endoxifen using the liver enzyme CYP2D6, which is the goal because the main metabolite is what does the anti estrogenic effects on selective tissue (such as the breast tissue and growth plates)
Endoxifen - 5mg daily
or
Tamoxifen - 20mg daily
Section 3: Steroids
TESTOSTERONE
Everyone knows this. Everyone knows it’s the base. Everyone wants it. So I won’t go into much detail in this page.
Your Testosterone should always be injected in the morning and it should be a low dose.
You guys can already guess that the low dose of Testosterone is primarily for the low E2 conversion… but that’s not all.
Letrozole.
Yes, Letrozole is the special factor here. In your growth plates, both Letrozole and Testosterone fight to take it over (this is all explained in simple terms btw). So you should be on lower dose Testosterone so more of the Letrozole occupies the growth plates.
This is why low test dosing was needed.
Your dosing should be sub 140mg weekly but even that is pushing it, in my opinion.
The ideal dosing for Testosterone should be 70-100mg, weekly. Yes. 70-100mg for the full week.
If you feel like fucking absolute shit on lower E2, you can raise your Testosterone dose, since your mental health in your teenage years matters more than your height in the end.
Now for the esters, and pinning.
The ideal for the ester is in the both ends of the spectrum. What does that mean?
For quick saturation, natural Testosterone shutdown, quick dose changes, and to be able to quickly change
TRENBOLONE
Tren is a very interesting compound. I think everyone already knows, but people don't know how important it is for height.
Tren synergizes well with low E2 due to its dopaminergic effects, it increases IGF-1 expression AND IGF-1 signaling essentially making GH more effective.
It has its androgenic signaling influences obviously but it also has increases in protein synthesis, nutrient partitioning, helps a tremendously with physique, the CNS drive gives absurd motivation and doesn't aromatize along with so many other things. Essentially this is an ideal compound, a compound that enhances the growth that is already happening AND pushes growth on its own. That is amazing.
There also is a bit of an issue with Tren.
With Tren, there is an effect where E2 ends up having higher estrogen like effects while the serum levels doesn't change. For example, having low E2 but taking Tren will give you maybe moderate E2 or maybe a bit below like effects. So essentially same concentrate but way larger effect. If you remember, we want to stay in a low E2 environment. So this is why crushing E2 is mandatory.
You want to microdose T3 and T4 as natural levels will be affected from the thyroid suppression from Tren. (Do not dose T3 and T4 too high as it will damage plates and that is what we have been trying to prevent.)
35mg-210mg weekly
MASTERON
Masteron, what is it?
Masteron, otherwise known as Drostanalone is a DHT derived steroid made for women's' breast cancer, but later the women ended up getting androgenic effects.
Masteron is a really special compound (I know I hate on it a lot) because of an enzyme called 3aHSD.
What is 3aHSD?
3aHSD is an enzyme that rapidly converts DHT into inactive metabolites inside muscle and skeletal tissue. Now, that doesn't mean that DHT itself is a bad hormone, but in this situation, DHT-derivatives are more resistant to the enzyme, causing a stronger effect on skeletal tissue and depending on the compound, a stronger effect on muscle.
I do want to note that there is a genetic part in this that comes into play (well, all things are based off your genes), your own bodies strength, amount and selectivity of this enzyme also does determine this. Such as how much of the enzyme is in the hair follicles or in the bone/muscle.
Masteron actually resists this enzyme which allows it to be able to have more anabolic and osteoanabolic activity at the price of sacrificing some androgenic activty.
200-800mg weekly
Dihydrotestosterone, what is it?
DHT, the hormone that makes us a man, the hormone that is the cause of puberty, the hormone that is the cause of growth spurts, the hormone that is the cause of... you get it.
DHT binds to the AR pretty strongly, and not as much as you think is needed. An average man makes 9mg of dht monthly, even taking 15mg is supraphysiological levels.
Proviron is closely related to DHT. It is DHT just made oral. So the changes you would get would be close to taking DHT. So if you want it, take DHT.
35mg-250mg DHT E/P
Section 4: Bioregulators
EPITALON
A synthetic tetrapeptide.
Slowing down cellular aging.
You know what that means.
So the senescence of growth plates is caused when resting zone chondrocytes reach the hayflick limit and can no longer duplicate the cell cycle of the growth plate going, estrogen speeds this up by rapidly cycling the RSC until they hit the hayflick limit.
We already established that not having an aromatase deficiency means you lost permanent replicate capacity.
What does that mean and what do we do about it?
Epitalon.
You can regain some of it using Epitalon.
because normal Epitalon is metabolized quickly, N-Acetyl group makes it resistant to the enzymes that breaks it down meaning longer and larger effect. Epitalon does this by activating hTERT human telomerase reverses transcriptase which tells the cell to make telomerase but interestingly it modulates it well, increasing it but not in a way that generates cancer.
VILON
A synthetic dipeptide.
Vilon has been studied for the immune system. Now, why is that beneficial? Why is THAT in THIS stack?
Vilon appears to influence gene expression involved in immune regulation and cellular homeostasis, helping cells behave more like they're supposed to. Now that is an AMAZING thing. Why does that matter though?
Because chronic inflammation and immune dysfunction accelerate aging, as in accelerate growth plate closure and will basically force your to already take Epitalon because of the dysfunction your cells MAY already have because of past gear usage. Do not let your body reduce your it's ability to repair itself. Take Vilon.
An easy understandable wrap up I can give is, if Epitalon is focused on the cell's lifespan then Vilon is focused on the environment those cells have to live in.
Hope that makes sense.
1mg year round, time of taking doesn't matter
VESUGEN
A synthetic dipeptide
Every tissue relies on your blood and blood vessels, so if they're not doing good, then you're not growing good.
I don't need to emphasize how important blood vessel health is, but it is your main driver of oxygen (here is a study where increased oxygen gave more mandible growth in rats), your main driver of nutrients, your main driver of hormones. Having healthy blood vessels is SO important, even if you aren't currently heightmaxing.
2mg daily year round
CARTALAX
A synthetic tripeptide.
For heightmaxing, cartilage is extremely important because you growth plates are made of specialized cartilage,. Health cartilage cells are responsible for producing the tissue that eventually becomes new bone during phases of growth.
Maintaining healthy cartilage and supporting chondrocyte function is detrimental for creating a better environment for cartilage based tissue to function and grow properly.
2mg daily 10 days on 20 days off
KARTOGENIN
A small molecule, not a peptide surprisingly.
Sounds very exciting, even more exciting when you realize your growth plates are made almost entirely of cartilage.
More healthy cartilage cells = more cartilage tissue = more bone during endochondral ossification
30-35mg
Section 5: PTH Analogs
TERIAPARATIDE
Teriparatide is a very interesting compound.
Most people know its for osteoporosis patients but they don't really understand how it actually works or why it matter (like now for instance) in a growth context.
Teriparatide is basically a fragment of Parathyroid hormone (PTH), specifically the active portion. Instead of elevating PTH like in hyperthyroidism (which breaks down bone), teriparatide works in a pulsatile manner which actually stimulates the bone formations.
What you read it very important.
When used correctly, teriparatide increases osteoblast activity. It also increases IGF-1, locally in bone tissue, which ties directly into growth signaling bone remodeling.
So this is what you get. Increased bone turnover, increased IGF-1 signaling in bone, improved bone density and structure.
This is very valuable however, there is a limitation.
Teriparatide does not directly "lengthen bones" but it also does. If plates are open... it will.
Issue is also this.
If the exposure to the PTH analog is too high, it shifts towards bone resorption instead of formation. This is why teriparatide is used in controlled, intermittent dosing.
ABALOPARATIDE
Abalo. Basically the same as Teriparatide but upgraded.
Most people also know that this is another medication for osteoporosis patients but they don't know how it is different or how it compares to Teriparatide when it is in a growth context.
Abaloparatide is a PTH analog that increases chondrocyte proliferation at the growth zone of the growth plate. The way in which it goes about doing this is more nuanced than the paracrine-related action that regular PTHrP acts by to enhance growth. Specifically, PTHrP is expressed in a spatial-gradient fashion, wherein it's expressed in periarticular / perichondral cells - Abaloparatide bypasses this by flooding your body with it. So then how is it good for height? It docks on PTH1R (endocrine-related) receptors in the RG conformation (transient phase), which biases towards formation over resorption.
This is where things get interesting.
Unlike Teriparatide, Abaloparatide has a slightly different receptor binding profile, it preferentially activates pathways that are most biased towards bone formation rather than resorption.
What does this mean?
More osteoblast activity.
Less stimulation of osteoclasts compared to a normal PTH
So an overall more "bone anabolic biased" effect.
80mcg every 24 hours, on the DOT. You will become desensitized overtime, =< 24 hours. You will increase bone loss if done incorrectly.
Section 5.5: PTH Synergy
ROMOSOZUMAB
(DO NOT TAKE THIS FOR HEIGHT IF EARLY ON IN PUBERTY)
(BEST IS TANNER STAGE 3)
Not really good for height, but its good for cortical thickening. Good overall though.
If used too early in the stack, you will prematurely mineralize your growth plates and cause them to close early.
If used in the latter half of puberty, it will benefit.
Romosozumab is a sclerostin inhibitor, which downstream disinhibits wnt/beta-catenin signaling in bone. In studies regarding its effects on osteoporosis, it has been shown to increase bone mineral density (BMD), and other such bone markers. For longitudinal bone growth, Romosozumab could theoretically work if and only if it's used in the latter half of puberty (i.e. the mineralization phase).
Sclerostin is basically a brake on bone formation. It inhibits Wnt/Beta-catenin pathway. This is one of the most powerful anabolic signaling pathways for bone growth.
So what happens?
Romosozumab removes that brake.
When sclerostin inhibited:
It increases bone formation WHILE decreasing bone resorption which is extremely rare.
105mg 2x a month (bi-monthly)
(210mg total for the whole month)
WAY316606
Don't take if Romosozumab is available.
Basically a carbon copy of Romosozumab, everything said before applies.
Titration will be needed at first, so follow the template below.
You will need to cycle WAY since there will be desensitization. Preferably 6 week breaks in between cycles. Any desensitization that could occur would be partially restored after 2 weeks, but we want full restoration, so we will wait for the full 6 weeks.
Beginner: 8-12mg daily (when osteocytes are most active is after you workout so ideally take post-workout.) (Stay in beginner for the first 4-8 weeks)
Intermediate: 12-24mg daily (Stay in intermediate 12-16 weeks)
Advanced: 24-48mg daily (Most don't ever need to get to this stage, running Intermediate cycles of WAY is already enough, but if you insist on running the Advanced cycle, run it for 12-16 weeks.)
KY19382
KY19382 — Wnt/β-catenin reactivator. Small-molecule CXXC5–DVL inhibitor that disrupts the CXXC5–Dvl interaction, stabilizes nuclear β-catenin, and reactivates Wnt signaling in the growth plate—effectively reversing senescence signaling. Mouse data (using 0.1mg/kg dosing) showed significant tibial elongation (p<0.0005), increasing the proliferation of chondrocytes, and expansion of the proliferative and hypertrophic growth zone; also promotes facial bone remodeling via periosteal apposition. Administration: subcutaneous preferred over transdermal. Caveats: entirely preclinical (mouse/cell), no human height trials, and Wnt activation carries theoretical cancer risk (though some models show context-dependent anti-tumor effects).
https://pmc.ncbi.nlm.nih.gov/articles/PMC6458850/
HED = animal dosage x ((Km of mouse)/(Km of human))
So in this situation it will look this
(0.1mg/kg) x (3/37) = 0.0081mg/kg
Now we have our dosages with the kg, time to applier our own weight.
Body Weight and HED needed for the weight.
Section 6: FGFR Inhibitors
INFIGRATINIB
Infigratinib — oral FGFR1–3 inhibitor. RCT data in achondroplasia showed +1.74–2.50 cm/year increase in annualized height velocity vs placebo, along with improved body proportionality (first drug to demonstrate this). The issue: lack of selectivity (FGFR1/2 inhibition) leads to hyperphosphatemia and added off-target toxicity. More clinically validated than TYRA-300, but comes with higher risk. https://investor.bridgebio.com/news...roportionality-in-Achondroplasia/default.aspx
ERDAFITINIB
Erdafitinib — pan-FGFR1–4 inhibitor, highly potent but least selective. A case report in a child treated for cancer showed extreme height velocity, but also rapid overgrowth, kyphoscoliosis, and spinal deformities (scoliosis). Mechanism is clearly effective, but the safety profile is the worst in this class. Not recommended. https://www.sciencedirect.com/science/article/pii/S2405844024069184
DAGORATINIB
TYRA-300 (Dabogratinib) — selective FGFR3-only inhibitor, first-in-class. Preclinical mouse data showed significant increases in femur (+3.7–5%) and tibia length (+3.75–6%), along with improved skeletal proportionality, even in wild-type (normal) mice — not just ACH models. This is important because it suggests potential benefit without a pathological FGFR3 mutation. It spares FGFR1/2/4, avoiding the phosphate toxicity seen with less selective drugs like infigratinib. Main issues: no human height trial data yet, hard to verify purity from gray-market sources, and high cost. https://insight.jci.org/articles/view/189307
Here is the thing, this is rat data only too, the human adult testing was for bladder cancer and the human child was for achondoplasia. Only the rats were used for bone growth, but here is the HED (Human Equivalent Dosage): 0.15mg/kg (low dose restoration of signaling) 0.65mg/kg (significant bone length increase in (in mice, using mouse dose)) 1.14mg/kg (high-end preclinical growth dose)
Section 7: CNP
Vosoritide - The first FDA-approved pharmaceutical to increase height in pediatric patients with achondroplasia. Vosoritide is a synthetic version of CNP but upgraded. It hade an extra amino acid tail so it survives 10x longer in the body. For example, the normal CNP in your body lasts 2 minutes, Vosoritide lasts 20 minutes. The way it works is that it hits the NPR-B receptor on cartilage cells (chondrocytes), the hit spikes the cGMP levels inside the cell which later directly block the Raf-1, what the FGFR3 uses to stop growth. In kids, this adds roughly 1.57cm per year of growth velocity over their baseline. This growth was shown on studied over a 7+ year period, starting AND staying on 15 micrograms/kg through the whole clinical trials. The 121 kids maintained an increased growth rate year-over-year as long as they stayed on the CNP. Now the data on kids have been from ages 5-15 years old.
15mcg/kg daily subq
Section 8: Oral Steroids
Fluoxymesterone (Halotestin)
Fluoxymesterone (Halotestin) — ~2.5 mg/day. Non-aromatizing (doesn’t convert to estrogen). Provides strong AR stimulation; may increase local IGF-1 receptor expression and sensitivity of chondrocytes to GH. A 1993 study in boys with growth delay reported increased growth and a higher final height vs predicted, with bone age advancing less than growth velocity.
Important caveats: evidence is limited/old, and effects on final height are inconsistent across contexts. Despite being non-aromatizing, androgens can still influence maturation and carry systemic risks. Fluoxymesterone is notably hepatotoxic and has adverse lipid and cardiovascular effects. Any use outside medical supervision is high-risk. It is very important that you cycle this compound, it is very toxic on the body.
2.5-10mg daily (injectable)
WINSTROL (STANZOLOL)
Winstrol (Stanazolol) — Non-aromatizing (doesn’t convert to estrogen). Provides strong AR stimulation; anti catabolic and SHBG suppressive while being a testosterone derivative. Has very unique properties such as being anticatabolic, increasing tissue healing via Sox9 and TGF beta, both being beneficial for height. Important caveats: Height evidence is extremely limited and old, and effects on final height are inconsistent across contexts. Despite being non-aromatizing, androgens can still influence maturation and carry systemic risks because of an increase in bone age. Stanazolol is also notably hepatotoxic and has adverse lipid and cardiovascular effects. Any use outside medical supervision is high-risk.
17.5mg (injectable)
or
25mg (oral)
ANAVAR (OXANDROLONE)
Oxandrolone (Anavar) — dosed around 2.5–5 mg/day, the mildest of the group. Has some pediatric ISS data. Minimal aromatization and can reduce aromatizable substrate via HPTA suppression. One study showed increased height velocity, but also accelerated skeletal age—some subjects lost ~1.5–7.5 cm of predicted adult height. So while growth rate increases, it may not improve final height. More evidence than Halotestin, but weaker risk/reward if the goal is maximizing height.
https://www.jpeds.com/article/S0022-3476(71)80204-4/fulltext
2.5-5mg daily
Heightmaxing is not a single method, but a combination of targeting multiple biological pathways that regulate growth. This includes both stimulating mechanism that promote height, and minimizing or delaying the factors that limit it. (Do remember that genetics play a big role in this)
The goal is to shift the body into a more growth-favorable state. Supporting process like growth signaling, while attempting to reduce constraints such as premature growth plate senescence and hormonal limitations. This is extremely important because we are living in a highly hormonal disruptive environment.
While some factors are fixed, others may be influenced to a degree. Understanding where intervention is possible and where it is not is the key to approaching this in a safer, efficient and more structured way.
Do understand that while some of these have been proven anecdotally and in the medical field, a chunk of it is theoretical framework based on known mechanisms, not everything is guaranteed.
Before you also get into the rest of the guide. You can already tell this is high effort. It is high effort for a reason. You're messing with growth pathways, with things even acting as growth limiter inhibitors. There is a risk of cancer.
Section 1: GH Axis
I was going to say...
But I can't say
Because that not an opinion OR an option. That is the truth.
All heightmaxing stacks start with HGH.
Growth hormone lowers certain breaks that are negative for height, while also working positively for height. While many people claim diminishing returns at 6-8iu daily, this is EXTREMELY irrelevant. We want quite literally as much as we can afford. It is so irrelevant that there is actually a rule associated with this. The rule of gear and especially GH is as high as you can tolerate and as much as you can afford.
There is also a specific study, can't find it right now but will link it later down the line. But summed up..
There was mice with no GH receptors (which also means they had no IGF-1) grew 60% less, while the mice with only no IGF-1 grew 33% less. Proving that GH is just as important as IGF-1.
8iu minimum, ideally you would go way higher. You will pin this 3 hours after eating, and 1-2 hours later eat a meal with carbs and protein, then you will go to sleep.
Here is an example timeline:
5pm: Eat meal --> 8pm: Pin --> 9-10pm: Eat carb and protein meal ---> Sleep
Just to reiterate for you
8iu MINIMUM
5pm: eat
8pm: pin
9-10pm: eat carb and protein
Then sleep.
GHRP’s
GHRPs, what are they?
GHRP stands for Growth Hormone Releasing Peptide. A synthetic peptide made to have your body release growth hormone by activating the ghrelin receptor. Some people know this as the growth hormone secretagogue receptor, or for short GHSR-1a.
What does this mean?
Well first of all, it is a GH releasing peptide, so it will release more GH along side the natural pulses your pituitary gland makes. The way this works is with the ghrelin receptor, what that also means is that you will be extremely hungry. Some GHRPs are stronger, some are weaker.
The oldest GHRP made, and its pretty well known. It's most well known for causing a very strong increase in appetite, with many people becoming noticeably hungrier within 15–30 minutes of taking it, making it popular for bulking or for those who struggle to eat enough. It also releases a pretty strong amount of GH. The most common side effects are intense hunger, a temporary feeling of warmth or flushing, and mild increases in prolactin and cortisol in some people.
A stronger version of GHRP-6, but not when it comes to appetite, but the strength of GH release it does is stronger than GHRP-6. Basically GHRP-6 with a stronger GH release and less appetite. This is ideal for GH release while GHRP-6 is ideal for more of an appetite.
Considered one of the most potent GHRPs. Producing larger growth hormone pulses than GHRP-2, GHRP-6, or Ipamorelin in many studies. Unlike GHRP-6, it usually causes little to no increase in appetite, making it a popular option for those who want stronger GH release without feeling constantly hungry. Same sides as before except desensitization of the ghrelin receptor with prolonged continuous use.
Like the other GHRPs, it increases natural GH pulses rather than supplying growth hormone directly, but it is known for being much more selective, causing little to no increase in prolactin, cortisol, or appetite at typical doses. The most common side effects are mild and may include temporary warmth or flushing, with significantly fewer hormonal side effects compared to GHRP-2, GHRP-6, or Hexarelin.
Pick either one, I personally would say GHRP would be better applicable in a theoretical heigh focused setting because of the receptor desensitization from Hexarelin.
GHRP-2: 500mcg split morning/night (250mcg morning and night)
Hexarelin: 200mcg split morning/night
GHRH’s
Growth Hormone-Releasing Hormone (GHRH) are peptides that increase growth hormone release by activating the GHRH receptor on the pituitary gland. Unlike GHRPs, which stimulate the ghrelin receptor, GHRH analogs work through the body's normal growth hormone signaling pathway, encouraging the pituitary to release its own natural GH. Their biggest advantage is that they produce natural, physiological pulses of growth hormone while preserving the body's normal feedback mechanisms, making their release pattern more similar to how GH is produced naturally.
One of first widely used GHRH analogs and shortest fully active fragment of GHRH. It makes a brief but solid GH pulse that closely matches natural physiology. But due to its very short half life, it's not ideal for growth.
First of all before I explain what No DAC or DAC is, I will explain what CJC-1295 is. CJC-1295 is a modified version of Sermorelin, it contains amino acid substitutions that significantly improve resistance to enzymatic breakdown. This results in a stronger, longer and more sustainable GH pulse.
Now what is DAC and what's the difference? DAC is basically like an ester, or if you know more about insulin then it is how fast/long acting it is. DAC stands for Drug Affinity Complex, which when attached to a peptide (such as CJC-1295) it allows it to bind to serum albumin and remain active for around one week. So what does this mean?
CJC No DAC = Upgraded sermorelin, in longer and stronger pulses.
Ex: turning on and off a faucet immediately
CJC With DAC = Upgraded Sermorelin, stronger but not in pulses, lasts a week.
Ex: letting a faucet drip over time
One of the most clinically backed GHRH analogs. It is a stabilized derivative that also maintains pulsatile secretion. Basically getting a 2 in 1.
CJC No DAC: 300mcg split morning and night
GHS-1RAs
Now, this is the one people know a lot about mainly because of one compound in there. I haven't mentioned it at all so far, so you can probably guess what it is. But before that lets explain GHS a bit.
GHS-R1a Agonists - compounds that activate Growth Hormone Secretagogue Receptor (GHS-R1a), commonly known as the ghrelin receptor. This receptor is one of the primary pathways the body uses to increase growth hormone output.
Now, you already know GHRHs activates the GHRH receptor but GHS-R1a agonists work by stimulating the ghrelin receptor while also reducing the effects of somatostatin, a hormone that normally suppresses growth hormone release. This dual mechanism produces larger, more powerful GH pulses, making them some of the strongest stimulators of your body's natural growth hormone production.
There is 2 different option, but I won't even list the other one just because of how strongly the other option mogs.
And you guys have been thinking it the whole time. Insulin resistance speedrun, severe hunger in a pill, HGH levels of sleep. You know exactly what I am talking about.
MK-677 is one of the most well known, if not, THE most well known secretagogue. Popular for it being a non injectable, non peptide GHS-R1a agonist. It is orally active, doesn't cause liver stress and remains active for around 24 hours.
This makes MK-677 one of the easiest options for increases your body's GH levels since it is extremely easily sourced, not injectable, can be in a liquid solution or a pill, and it is a easy once a day dosing.
(obviously) MK-677: 15-50mg daily, before bed or morning, either one is fine (dose is dependent on full GH axis stack)
Synergy
HGH → Provides a steady baseline of circulating GH
GHRH analog → Stimulates the pituitary through the GHRH receptor
GHRP → Amplifies pituitary GH release via the ghrelin receptor and reduced somatostatin activity
GHSR-1a agonist → Further activates the ghrelin pathway
So imagine all of that together.
Ideal GH axis would be this (itll be relisted theoretical stack):
HGH
GHRP-2/Ipamorelin
CJC No Dac
MK-677
Section 2: Estrogen/E2
This is one of the most controversial ones people talk about when it comes to height. Mainly because people claim there is a very large amount of draw backs (and I agree, there is.) of Letrozole 2.5mg. It is taken right after injecting Testosterone, or Aromasin 12.5mg, ideally 25mg every day taken right after injecting Testosterone on an empty stomach.
We want to make sure that our e2 is LOW.
Now since you read that you will be making claims about brain development.
Your brain actually never stops developing and has a multitude of catchup mechanisms if it occurs. It occurs if brain development is disrupted. But you don't need to worry about that because these compounds do not have the effect on the brain that you think they do.
If you ARE worried about missing brain development, you can take Arimidex instead, there is an enzyme that transports it out of the brain, resulting in the lowest blood concentration to brain concentration of an AI, so you can have higher localized e2 with aromasin.
So best is Letrozole or Arimidex. Pick your poison.
There are a bunch of common misconceptions and not fully correct thought process that people also have. It will be mentioned and explained below.
First of all, exorbitant doses (this will be talked about in the Testosterone section) are not ideal at all.
Bone resorption only occurs in negligible parts of growth and health.
Lowers IGF-1, yes it does. But not by a lot. Around the average of 50ng.
Now in turn, this is what you get.
MONTHS of extra growth.
Less limits.
Mental and mood benefits.
(You will be depressed to hell if ran without test)
Estrogen has been damaging your plates. Yes it has. And it has been damaging them for YEARS.
It doesn't matter if you have 100 E2 or 0 E2 because in the end your plates will close (obviously 0 E2 is better, just trying to prove a point). You plates WILL close in the end, this is a process we can not reverse. Another process you can't reverse, or at least fully, is the plate damage it has done, if we could reverse it fully then we would all be 9ft Chads but that's not happening... because our cells already knows estrogen exists, so it will get detected and issues arise.
But for every problem, there is a solution. Or at least a treatment.
It will be listed later in the module.
Serms
A SERM is a Selective Estrogen Receptor Modulator. What it does is it binds to estrogen receptors and blocks estrogen's effects in certain tissues, while acting differently in others. This one will be split into two since I have two things I want to talk about. Let's get into it.
Endoxifen - the main active metabolite of tamoxifen. Tamoxifen has to be converted into endoxifen by the liver enzyme CYP2D6, so having endoxifen itself will bypass this issue because some people have genetic variants that make CYP2D6 work poorly, so they produce much less endoxifen and may receive less benefit from tamoxifen.
Tamoxifen - also known as the brand the Nolvadex. Same situation as Endoxifen. Tamoxifen converts into Endoxifen using the liver enzyme CYP2D6, which is the goal because the main metabolite is what does the anti estrogenic effects on selective tissue (such as the breast tissue and growth plates)
Endoxifen - 5mg daily
or
Tamoxifen - 20mg daily
Section 3: Steroids
TESTOSTERONE
Everyone knows this. Everyone knows it’s the base. Everyone wants it. So I won’t go into much detail in this page.
Your Testosterone should always be injected in the morning and it should be a low dose.
You guys can already guess that the low dose of Testosterone is primarily for the low E2 conversion… but that’s not all.
Letrozole.
Yes, Letrozole is the special factor here. In your growth plates, both Letrozole and Testosterone fight to take it over (this is all explained in simple terms btw). So you should be on lower dose Testosterone so more of the Letrozole occupies the growth plates.
This is why low test dosing was needed.
Your dosing should be sub 140mg weekly but even that is pushing it, in my opinion.
The ideal dosing for Testosterone should be 70-100mg, weekly. Yes. 70-100mg for the full week.
If you feel like fucking absolute shit on lower E2, you can raise your Testosterone dose, since your mental health in your teenage years matters more than your height in the end.
Now for the esters, and pinning.
The ideal for the ester is in the both ends of the spectrum. What does that mean?
For quick saturation, natural Testosterone shutdown, quick dose changes, and to be able to quickly change
TRENBOLONE
Tren is a very interesting compound. I think everyone already knows, but people don't know how important it is for height.
Tren synergizes well with low E2 due to its dopaminergic effects, it increases IGF-1 expression AND IGF-1 signaling essentially making GH more effective.
It has its androgenic signaling influences obviously but it also has increases in protein synthesis, nutrient partitioning, helps a tremendously with physique, the CNS drive gives absurd motivation and doesn't aromatize along with so many other things. Essentially this is an ideal compound, a compound that enhances the growth that is already happening AND pushes growth on its own. That is amazing.
There also is a bit of an issue with Tren.
With Tren, there is an effect where E2 ends up having higher estrogen like effects while the serum levels doesn't change. For example, having low E2 but taking Tren will give you maybe moderate E2 or maybe a bit below like effects. So essentially same concentrate but way larger effect. If you remember, we want to stay in a low E2 environment. So this is why crushing E2 is mandatory.
You want to microdose T3 and T4 as natural levels will be affected from the thyroid suppression from Tren. (Do not dose T3 and T4 too high as it will damage plates and that is what we have been trying to prevent.)
35mg-210mg weekly
MASTERON
Masteron, what is it?
Masteron, otherwise known as Drostanalone is a DHT derived steroid made for women's' breast cancer, but later the women ended up getting androgenic effects.
Masteron is a really special compound (I know I hate on it a lot) because of an enzyme called 3aHSD.
What is 3aHSD?
3aHSD is an enzyme that rapidly converts DHT into inactive metabolites inside muscle and skeletal tissue. Now, that doesn't mean that DHT itself is a bad hormone, but in this situation, DHT-derivatives are more resistant to the enzyme, causing a stronger effect on skeletal tissue and depending on the compound, a stronger effect on muscle.
I do want to note that there is a genetic part in this that comes into play (well, all things are based off your genes), your own bodies strength, amount and selectivity of this enzyme also does determine this. Such as how much of the enzyme is in the hair follicles or in the bone/muscle.
Masteron actually resists this enzyme which allows it to be able to have more anabolic and osteoanabolic activity at the price of sacrificing some androgenic activty.
200-800mg weekly
Dihydrotestosterone, what is it?
DHT, the hormone that makes us a man, the hormone that is the cause of puberty, the hormone that is the cause of growth spurts, the hormone that is the cause of... you get it.
DHT binds to the AR pretty strongly, and not as much as you think is needed. An average man makes 9mg of dht monthly, even taking 15mg is supraphysiological levels.
Proviron is closely related to DHT. It is DHT just made oral. So the changes you would get would be close to taking DHT. So if you want it, take DHT.
35mg-250mg DHT E/P
Section 4: Bioregulators
EPITALON
A synthetic tetrapeptide.
(That above was stolen off the internet btw.)
Slowing down cellular aging.
You know what that means.
So the senescence of growth plates is caused when resting zone chondrocytes reach the hayflick limit and can no longer duplicate the cell cycle of the growth plate going, estrogen speeds this up by rapidly cycling the RSC until they hit the hayflick limit.
We already established that not having an aromatase deficiency means you lost permanent replicate capacity.
What does that mean and what do we do about it?
Epitalon.
You can regain some of it using Epitalon.
because normal Epitalon is metabolized quickly, N-Acetyl group makes it resistant to the enzymes that breaks it down meaning longer and larger effect. Epitalon does this by activating hTERT human telomerase reverses transcriptase which tells the cell to make telomerase but interestingly it modulates it well, increasing it but not in a way that generates cancer.
VILON
A synthetic dipeptide.
Not a bad thing to have as you get older, but even better if you're younger.
Vilon has been studied for the immune system. Now, why is that beneficial? Why is THAT in THIS stack?
Vilon appears to influence gene expression involved in immune regulation and cellular homeostasis, helping cells behave more like they're supposed to. Now that is an AMAZING thing. Why does that matter though?
Because chronic inflammation and immune dysfunction accelerate aging, as in accelerate growth plate closure and will basically force your to already take Epitalon because of the dysfunction your cells MAY already have because of past gear usage. Do not let your body reduce your it's ability to repair itself. Take Vilon.
An easy understandable wrap up I can give is, if Epitalon is focused on the cell's lifespan then Vilon is focused on the environment those cells have to live in.
Hope that makes sense.
1mg year round, time of taking doesn't matter
VESUGEN
A synthetic dipeptide
Basically keeping your blood vessels longer. Doesn't sound very exciting until you realize your whole body relies on it.
Every tissue relies on your blood and blood vessels, so if they're not doing good, then you're not growing good.
I don't need to emphasize how important blood vessel health is, but it is your main driver of oxygen (here is a study where increased oxygen gave more mandible growth in rats), your main driver of nutrients, your main driver of hormones. Having healthy blood vessels is SO important, even if you aren't currently heightmaxing.
2mg daily year round
CARTALAX
A synthetic tripeptide.
Basically what it does it keep your cartilage healthier for longer. Doesn't sounds very exciting until you remember what the base of all longitudinal bone growth comes from.
For heightmaxing, cartilage is extremely important because you growth plates are made of specialized cartilage,. Health cartilage cells are responsible for producing the tissue that eventually becomes new bone during phases of growth.
Maintaining healthy cartilage and supporting chondrocyte function is detrimental for creating a better environment for cartilage based tissue to function and grow properly.
2mg daily 10 days on 20 days off
KARTOGENIN
A small molecule, not a peptide surprisingly.
Unlike peptides like Cartalax, which is made to support the function of existing cartilage cells. Kartogenin is completely different. Kartogenin encourages the formation of new cartilage cells by activating pathways in chondrogenesis. Basically telling stem cells to become cartilage cells.
Sounds very exciting, even more exciting when you realize your growth plates are made almost entirely of cartilage.
More healthy cartilage cells = more cartilage tissue = more bone during endochondral ossification
30-35mg
Section 5: PTH Analogs
TERIAPARATIDE
Teriparatide is a very interesting compound.
Most people know its for osteoporosis patients but they don't really understand how it actually works or why it matter (like now for instance) in a growth context.
Teriparatide is basically a fragment of Parathyroid hormone (PTH), specifically the active portion. Instead of elevating PTH like in hyperthyroidism (which breaks down bone), teriparatide works in a pulsatile manner which actually stimulates the bone formations.
What you read it very important.
When used correctly, teriparatide increases osteoblast activity. It also increases IGF-1, locally in bone tissue, which ties directly into growth signaling bone remodeling.
So this is what you get. Increased bone turnover, increased IGF-1 signaling in bone, improved bone density and structure.
This is very valuable however, there is a limitation.
Teriparatide does not directly "lengthen bones" but it also does. If plates are open... it will.
Issue is also this.
If the exposure to the PTH analog is too high, it shifts towards bone resorption instead of formation. This is why teriparatide is used in controlled, intermittent dosing.
ABALOPARATIDE
Abalo. Basically the same as Teriparatide but upgraded.
Most people also know that this is another medication for osteoporosis patients but they don't know how it is different or how it compares to Teriparatide when it is in a growth context.
Abaloparatide is a PTH analog that increases chondrocyte proliferation at the growth zone of the growth plate. The way in which it goes about doing this is more nuanced than the paracrine-related action that regular PTHrP acts by to enhance growth. Specifically, PTHrP is expressed in a spatial-gradient fashion, wherein it's expressed in periarticular / perichondral cells - Abaloparatide bypasses this by flooding your body with it. So then how is it good for height? It docks on PTH1R (endocrine-related) receptors in the RG conformation (transient phase), which biases towards formation over resorption.
This is where things get interesting.
Unlike Teriparatide, Abaloparatide has a slightly different receptor binding profile, it preferentially activates pathways that are most biased towards bone formation rather than resorption.
What does this mean?
More osteoblast activity.
Less stimulation of osteoclasts compared to a normal PTH
So an overall more "bone anabolic biased" effect.
80mcg every 24 hours, on the DOT. You will become desensitized overtime, =< 24 hours. You will increase bone loss if done incorrectly.
Section 5.5: PTH Synergy
ROMOSOZUMAB
(DO NOT TAKE THIS FOR HEIGHT IF EARLY ON IN PUBERTY)
(BEST IS TANNER STAGE 3)
Not really good for height, but its good for cortical thickening. Good overall though.
If used too early in the stack, you will prematurely mineralize your growth plates and cause them to close early.
If used in the latter half of puberty, it will benefit.
Romosozumab is a sclerostin inhibitor, which downstream disinhibits wnt/beta-catenin signaling in bone. In studies regarding its effects on osteoporosis, it has been shown to increase bone mineral density (BMD), and other such bone markers. For longitudinal bone growth, Romosozumab could theoretically work if and only if it's used in the latter half of puberty (i.e. the mineralization phase).
Sclerostin is basically a brake on bone formation. It inhibits Wnt/Beta-catenin pathway. This is one of the most powerful anabolic signaling pathways for bone growth.
So what happens?
Romosozumab removes that brake.
When sclerostin inhibited:
- Wnt signaling is increased
- Osteoblast activity is increased
- Bone formation and bone matrix support is increased significantly
It increases bone formation WHILE decreasing bone resorption which is extremely rare.
105mg 2x a month (bi-monthly)
(210mg total for the whole month)
WAY316606
Don't take if Romosozumab is available.
Basically a carbon copy of Romosozumab, everything said before applies.
Titration will be needed at first, so follow the template below.
You will need to cycle WAY since there will be desensitization. Preferably 6 week breaks in between cycles. Any desensitization that could occur would be partially restored after 2 weeks, but we want full restoration, so we will wait for the full 6 weeks.
Beginner: 8-12mg daily (when osteocytes are most active is after you workout so ideally take post-workout.) (Stay in beginner for the first 4-8 weeks)
Intermediate: 12-24mg daily (Stay in intermediate 12-16 weeks)
Advanced: 24-48mg daily (Most don't ever need to get to this stage, running Intermediate cycles of WAY is already enough, but if you insist on running the Advanced cycle, run it for 12-16 weeks.)
KY19382
KY19382 — Wnt/β-catenin reactivator. Small-molecule CXXC5–DVL inhibitor that disrupts the CXXC5–Dvl interaction, stabilizes nuclear β-catenin, and reactivates Wnt signaling in the growth plate—effectively reversing senescence signaling. Mouse data (using 0.1mg/kg dosing) showed significant tibial elongation (p<0.0005), increasing the proliferation of chondrocytes, and expansion of the proliferative and hypertrophic growth zone; also promotes facial bone remodeling via periosteal apposition. Administration: subcutaneous preferred over transdermal. Caveats: entirely preclinical (mouse/cell), no human height trials, and Wnt activation carries theoretical cancer risk (though some models show context-dependent anti-tumor effects).
https://pmc.ncbi.nlm.nih.gov/articles/PMC6458850/
The dosing and protocol that produced the beneficial effects on mice was:
- 0.1 mg/kg
- Intraperitoneal (i.p.)
- Once daily
- 2 weeks (for growth plate histology)
- 10 weeks (for increased tibial length)
HED = animal dosage x ((Km of mouse)/(Km of human))
So in this situation it will look this
(0.1mg/kg) x (3/37) = 0.0081mg/kg
Now we have our dosages with the kg, time to applier our own weight.
Body Weight and HED needed for the weight.
- 60kg
- 0.49 mg
- 0.57 mg
Section 6: FGFR Inhibitors
INFIGRATINIB
Infigratinib — oral FGFR1–3 inhibitor. RCT data in achondroplasia showed +1.74–2.50 cm/year increase in annualized height velocity vs placebo, along with improved body proportionality (first drug to demonstrate this). The issue: lack of selectivity (FGFR1/2 inhibition) leads to hyperphosphatemia and added off-target toxicity. More clinically validated than TYRA-300, but comes with higher risk. https://investor.bridgebio.com/news...roportionality-in-Achondroplasia/default.aspx
ERDAFITINIB
Erdafitinib — pan-FGFR1–4 inhibitor, highly potent but least selective. A case report in a child treated for cancer showed extreme height velocity, but also rapid overgrowth, kyphoscoliosis, and spinal deformities (scoliosis). Mechanism is clearly effective, but the safety profile is the worst in this class. Not recommended. https://www.sciencedirect.com/science/article/pii/S2405844024069184
- Average Dosing:
- 4mg-6mg (stick to 4mg or under)
DAGORATINIB
TYRA-300 (Dabogratinib) — selective FGFR3-only inhibitor, first-in-class. Preclinical mouse data showed significant increases in femur (+3.7–5%) and tibia length (+3.75–6%), along with improved skeletal proportionality, even in wild-type (normal) mice — not just ACH models. This is important because it suggests potential benefit without a pathological FGFR3 mutation. It spares FGFR1/2/4, avoiding the phosphate toxicity seen with less selective drugs like infigratinib. Main issues: no human height trial data yet, hard to verify purity from gray-market sources, and high cost. https://insight.jci.org/articles/view/189307
Here is the thing, this is rat data only too, the human adult testing was for bladder cancer and the human child was for achondoplasia. Only the rats were used for bone growth, but here is the HED (Human Equivalent Dosage): 0.15mg/kg (low dose restoration of signaling) 0.65mg/kg (significant bone length increase in (in mice, using mouse dose)) 1.14mg/kg (high-end preclinical growth dose)
Section 7: CNP
Vosoritide - The first FDA-approved pharmaceutical to increase height in pediatric patients with achondroplasia. Vosoritide is a synthetic version of CNP but upgraded. It hade an extra amino acid tail so it survives 10x longer in the body. For example, the normal CNP in your body lasts 2 minutes, Vosoritide lasts 20 minutes. The way it works is that it hits the NPR-B receptor on cartilage cells (chondrocytes), the hit spikes the cGMP levels inside the cell which later directly block the Raf-1, what the FGFR3 uses to stop growth. In kids, this adds roughly 1.57cm per year of growth velocity over their baseline. This growth was shown on studied over a 7+ year period, starting AND staying on 15 micrograms/kg through the whole clinical trials. The 121 kids maintained an increased growth rate year-over-year as long as they stayed on the CNP. Now the data on kids have been from ages 5-15 years old.
15mcg/kg daily subq
- 60kg
- 900 mcg (0.90 mg)
- 975 mcg (0.975 mg)
- 80kg
Section 8: Oral Steroids
Fluoxymesterone (Halotestin)
Fluoxymesterone (Halotestin) — ~2.5 mg/day. Non-aromatizing (doesn’t convert to estrogen). Provides strong AR stimulation; may increase local IGF-1 receptor expression and sensitivity of chondrocytes to GH. A 1993 study in boys with growth delay reported increased growth and a higher final height vs predicted, with bone age advancing less than growth velocity.
Important caveats: evidence is limited/old, and effects on final height are inconsistent across contexts. Despite being non-aromatizing, androgens can still influence maturation and carry systemic risks. Fluoxymesterone is notably hepatotoxic and has adverse lipid and cardiovascular effects. Any use outside medical supervision is high-risk. It is very important that you cycle this compound, it is very toxic on the body.
2.5-10mg daily (injectable)
WINSTROL (STANZOLOL)
Winstrol (Stanazolol) — Non-aromatizing (doesn’t convert to estrogen). Provides strong AR stimulation; anti catabolic and SHBG suppressive while being a testosterone derivative. Has very unique properties such as being anticatabolic, increasing tissue healing via Sox9 and TGF beta, both being beneficial for height. Important caveats: Height evidence is extremely limited and old, and effects on final height are inconsistent across contexts. Despite being non-aromatizing, androgens can still influence maturation and carry systemic risks because of an increase in bone age. Stanazolol is also notably hepatotoxic and has adverse lipid and cardiovascular effects. Any use outside medical supervision is high-risk.
17.5mg (injectable)
or
25mg (oral)
ANAVAR (OXANDROLONE)
Oxandrolone (Anavar) — dosed around 2.5–5 mg/day, the mildest of the group. Has some pediatric ISS data. Minimal aromatization and can reduce aromatizable substrate via HPTA suppression. One study showed increased height velocity, but also accelerated skeletal age—some subjects lost ~1.5–7.5 cm of predicted adult height. So while growth rate increases, it may not improve final height. More evidence than Halotestin, but weaker risk/reward if the goal is maximizing height.
https://www.jpeds.com/article/S0022-3476(71)80204-4/fulltext
2.5-5mg daily