Increlex
mecasermin — recombinant human IGF-1
Increlex (mecasermin — recombinant human IGF-1) is a gh & growth research compound. Recombinant human IGF-1 itself, not a secretagogue. Everything upstream — GHRH analogs, ghrelin mimetics, growth hormone — exists to raise IGF-1. This is the endpoint delivered directly, which removes the liver's regulatory step and the negative feedback that comes with it.
Increlex quick facts
| Route | Subq |
| Frequency | 2x Daily |
| Half-life | ~5.8 hrs |
| Forms | Injectable |
| Evidence level | FDA-approved (severe primary IGF-1 deficiency); human |
The most consequential safety line in this batch: IGF-1 has real insulin-like activity, so HYPOGLYCEMIA is the dose-limiting risk and the label requires it be taken with a meal, not fasted. That single rule is the opposite of how most of the GH-axis compounds in the Vault are timed. Approved for a specific pediatric deficiency, and used far outside that.
How Increlex works
Recombinant human IGF-1 itself, not a secretagogue. Everything upstream — GHRH analogs, ghrelin mimetics, growth hormone — exists to raise IGF-1. This is the endpoint delivered directly, which removes the liver's regulatory step and the negative feedback that comes with it.
Proposed benefits
Researched for lean-mass support, recovery, sleep depth, connective-tissue repair and improved body composition via the GH/IGF-1 axis.
Where to get Increlex
See vetted vendors for Increlex →The evidence for Increlex
Graded by what exists behind each claim.
✅ Clinically validated
- FDA-approved (mecasermin) for severe primary IGF-1 deficiency. The label dose is 0.04-0.12 mg/kg twice daily, titrated up from the low end.
- Hypoglycemia is the dose-limiting adverse effect and it is on the label. IGF-1 has genuine insulin-like activity, which is why the approved instruction is to dose WITH a meal — the opposite of how most GH-axis compounds in this Vault are timed.
📊 Correlative data
- Long clinical use in a narrow pediatric population. Reported effects include tonsillar hypertrophy and injection-site lipohypertrophy — both consequences of sustained tissue-level IGF-1 rather than surprises.
🧪 Theoretical / extrapolated
- This is IGF-1 itself, not a secretagogue. Every GHRH analog and ghrelin mimetic in the Vault exists to raise IGF-1; this delivers the endpoint directly and removes the liver's regulatory step along with the negative feedback that comes with it.
- Bypassing that regulation is the entire risk profile in one sentence: there is no upstream brake left.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Increlex actually does
The single most important fact about injected IGF-1 is not what it does. It is what is missing alongside it. Endogenous IGF-1 does not circulate free. Roughly 75–80% of it is held in a 150 kilodalton ternary complex with insulin-like growth factor binding protein 3 and the acid-labile subunit, both of which are made by the liver under growth hormone control. Most of the remainder is bound to other binding proteins. Less than 1% is free. The ternary complex is too large to cross the capillary endothelium, so it functions as a circulating reservoir that extends IGF-1's half-life from minutes to many hours and keeps it out of the tissues until it is released LeRoith 2021.
Mecasermin is recombinant human IGF-1 with no binding protein. Injected on its own, it enters a system whose buffering capacity is already occupied — and in severe primary IGF-1 deficiency, where GH signaling is absent, IGFBP-3 and the acid-labile subunit are themselves low, so the buffer barely exists. The result is a much larger free fraction than the same nominal IGF-1 concentration would produce physiologically. Everything else on this page follows from that one sentence.
Because free IGF-1 is not selective for its own receptor. The IGF-1 receptor and the insulin receptor are homologous tyrosine kinases; they form hybrid receptors, and IGF-1 has real affinity for the insulin receptor at supraphysiological free concentrations. That is why hypoglycemia is the dose-limiting toxicity, why the drug is given with a meal rather than fasted, and why the schedule is twice daily rather than weekly. It is insulin-like activity, delivered by a molecule everyone files under growth.
And here is the fact that reorganizes the entire GH section of the Vault. Every secretagogue on this site — the GHRH analogs, the ghrelin mimetics, growth hormone itself — raises IGF-1 by raising GH. GH also raises IGFBP-3 and the acid-labile subunit. So those compounds raise the ligand and the buffer together, and IGF-1 goes up inside its complex. Injecting mecasermin raises the ligand alone. Two routes to the same number on a lab report, and completely different pharmacology — and the difference is measurable, because bioactive IGF-1 can be assayed separately from total Vilmann 2025.
Cell, rodent, human — and where it stops
Step one, in humans, because this is an approved medicine and the pediatric endocrinology literature is the primary source. Mecasermin's profile for long-term treatment of growth failure in severe primary IGF-1 deficiency is documented Fintini 2009, and near-adult height outcomes have now been reported from real-world registry data Ramon-Krauel 2025. The condition itself, and the difficulties of managing it, are described from a multi-stakeholder perspective Backeljauw 2023.
Step two, the safety number the Vault should be quoting. In the Eu-IGFD registry, 80 of 306 patients treated with rhIGF-1 experienced hypoglycemia. Those who did were younger at treatment start (8.7 versus 9.8 years) and more frequently had Laron syndrome (27.5% versus 10.3%); a prior history of hypoglycemia and a Laron diagnosis predicted future events Bang 2023. Roughly a quarter of a monitored, prescribed, pediatric-supervised population had a hypoglycemic event. That is the rate under medical supervision with a mandated meal rule.
Step three, the obstacle, and it is a population obstacle rather than a mechanism one. Every number above comes from children and adolescents with a genetic defect in GH signaling, dosed to grow. The people reading this page are metabolically intact adults with normal or high GH signaling, dosing for body composition. Two things change in that population and they change in opposite directions. The buffer is intact, so a given dose produces a smaller free fraction and the hypoglycemia risk per microgram is probably lower. But the feedback is also intact: exogenous IGF-1 suppresses pituitary GH secretion, which lowers hepatic IGFBP-3 and acid-labile subunit production, which shrinks the buffer over time — so the free fraction on a fixed dose can rise over weeks. Nobody has measured that trajectory in an adult using this off-label.
Increlex pharmacokinetics — how much of it actually gets in
The card says ~5.8 hours, which is right and is the most informative number on the page once you know what it is a half-life OF.
It is the half-life of IGF-1 that is only partly buffered. Free IGF-1 has a half-life measured in minutes. IGF-1 in the 150 kDa ternary complex has a half-life of 12–15 hours or more LeRoith 2021. The ~5.8 hour figure sits between those two, which is exactly what you would predict for a dose given into a system with reduced binding capacity: some is captured, some is not, and the observed number is a weighted average. The half-life is therefore a readout of how much buffer the patient has — which means it is not a fixed property of the drug, and it should differ between a Laron patient and a healthy adult. That prediction has never been tested.
What degrades it. IGF-1 is a 70-amino-acid protein cleared by proteolysis and by receptor-mediated internalization, with renal clearance of the free peptide contributing; there is no cytochrome involvement. The binding proteins are themselves cleared by specific proteases, so the buffer has its own turnover.
The oral barrier, and why the route is fixed. A 70-residue protein swallowed meets pepsin, trypsin and chymotrypsin and brush-border peptidases; oral bioavailability is effectively zero and first-pass metabolism is irrelevant because nothing reaches the portal circulation intact. Subcutaneous injection gives high bioavailability and a time-to-peak of roughly one to two hours.
The number that dictates the schedule, and it is a meal. Twice-daily dosing exists because a ~5.8 hour half-life cannot maintain exposure across a day, and the meal requirement exists because peak free IGF-1 arrives one to two hours after the injection — which has to coincide with absorbed carbohydrate, not with a fasted state. That is the exact opposite of how every growth hormone secretagogue in this Vault is timed, since those are dosed fasted to avoid blunting the GH pulse. A person who carries the fasted-injection habit across to this compound has inverted the one rule that matters, and the registry shows how common hypoglycemia is even when the rule is followed Bang 2023.
What would have to be true, and how you would know it was not
Three predictions. The second is the one that separates this compound from every secretagogue on the site; the third argues against it.
1. IGF-1 will rise and it will not tell you what you think. IGF-1 is the marker everyone orders, and a standard assay measures total, not free. Since injected mecasermin is unbuffered and GH-driven IGF-1 is buffered, the same total IGF-1 value means a different free concentration depending on how it was produced. Bioactive IGF-1 can be measured separately, and has been, in children on growth hormone Vilmann 2025. Prediction: on mecasermin, bioactive IGF-1 runs high relative to total; on a secretagogue, it tracks total. Nobody has published that comparison, and it would settle whether the two routes are interchangeable.
2. Fasting insulin and HbA1c should FALL, and that is the insulin-receptor arm becoming visible. Draw fasting insulin and HbA1c at baseline and 8 weeks. Prediction: fasting insulin falls, because exogenous IGF-1 does part of insulin's job and the pancreas responds by making less; HbA1c drifts down slightly. A falling fasting insulin here is not improved insulin sensitivity — it is a second agonist at the same receptor family, and reading it as sensitivity is the commonest misinterpretation of an IGF-1 panel.
3. The prediction that cuts against it: growth hormone should fall, and with it the buffer. IGF-1 is the negative feedback signal to the pituitary and hypothalamus. Draw growth hormone and IGF-1 at baseline and at 8 weeks. Prediction: GH suppressed. That matters because GH drives hepatic IGFBP-3 and acid-labile subunit synthesis LeRoith 2021 — so suppressing GH shrinks the buffer, which raises the free fraction of the next identical dose. The mechanism predicts that this drug becomes relatively more potent, and more hypoglycemic, the longer it is used at a fixed dose. That is the opposite of tolerance, it follows directly from the endocrinology, and no published study has measured it.
What nobody has tested yet
Four experiments that have never been run, and the first three are about the population actually reading this.
Nobody has measured the pharmacokinetics of mecasermin in a healthy adult. Every published figure comes from patients with severe primary IGF-1 deficiency, whose binding-protein status is abnormal by definition Backeljauw 2023. Since the half-life is a readout of buffer capacity, the number in an intact adult should be longer, and nobody has checked. Six timed draws after one dose would produce the first such dataset.
Nobody has tracked IGFBP-3 and the acid-labile subunit over weeks of exogenous IGF-1. The feedback argument above predicts the buffer shrinks. Both are measurable. If it is right, fixed-dose protocols get progressively more hypoglycemic and the correct protocol is a de-escalating one — which nobody does.
Nobody has compared bioactive IGF-1 between the injected and the secretagogue routes. The assay exists and has been used in children on GH therapy Vilmann 2025. The comparison would tell the whole GH section of this Vault whether ‘raising IGF-1’ means one thing or two.
Nobody has established whether continuous exposure is worse than pulsatile for the same total dose. Endogenous IGF-1 is relatively steady while GH is pulsatile, and the receptors downstream behave differently under the two patterns. Twice-daily injection is a schedule inherited from a growth indication, not one derived from an adult body-composition goal, and the alternative has never been tested.
Increlex — its own safety story, not its class's
Hypoglycemia is not one risk among several here. It is the dose-limiting toxicity, it has a measured frequency, and it dictates the entire administration protocol.
The number, from a real registry. 80 of 306 patients on rhIGF-1 had hypoglycemia; younger age at start and Laron syndrome predicted it, and prior hypoglycemia predicted more Bang 2023. That is a supervised population following a mandated meal rule. An unsupervised adult injecting fasted, before training, has removed the one control that population had. The signs — sweating, tremor, confusion, and in training a sudden inability to continue — are also the signs of a hard session, which is exactly the confusion that makes this dangerous.
Why the meal rule is a mechanism and not a convention. Peak free IGF-1 arrives one to two hours after injection. Carbohydrate has to be absorbed across that window, not before it. A dose taken with food and then followed by three hours of fasted training puts the peak in the wrong place, and the free fraction is the part that acts at the insulin receptor.
The growth-related risks, stated at the right size. IGF-1 is mitogenic, so the theoretical concerns are the ones any growth signal raises: tonsillar and adenoidal hypertrophy is a documented and sometimes surgical issue in the treated pediatric population Fintini 2009 Ramon-Krauel 2025, and lymphoid tissue anywhere responds to the same signal. Intracranial hypertension and slipped capital femoral epiphysis appear in the pediatric literature. The malignancy question has no answer either way in an adult population, because no such population has been followed.
The interaction that is easy to miss. Anything else that lowers glucose is additive with an insulin-receptor agonist — insulin obviously, but also the GLP-1 agonists that many readers of this Vault are already taking, and alcohol, which blocks hepatic gluconeogenesis. A GLP-1 agonist that has already reduced food intake, plus an unbuffered IGF-1 injection, plus a fasted morning, is three independent contributions to the same failure.
What reduces risk here, mechanistically. Not injection technique. The measures that follow from the pharmacology are: eat the meal, and eat it so absorption spans the one-to-two-hour peak; carry fast carbohydrate; do not train fasted on a dosing day; and treat any dose escalation as an escalation of insulin-like activity rather than of anabolic signal. Increlex is a prescription medicine for a specific pediatric deficiency, and nothing here is medical advice or a recommendation for use.
Sources read for this page
- Bang P, et al. Frequency and Predictive Factors of Hypoglycemia in Patients Treated With rhIGF-1: Data From the Eu-IGFD Registry. Journal of Clinical Endocrinology and Metabolism 2023 · PMID 37579214
- Ramon-Krauel M, et al. Near-Adult Height Outcomes in Patients Treated With rhIGF-1 for Severe Growth Failure: Real-World IGFD Registry Data. Journal of Clinical Endocrinology and Metabolism 2025 · PMID 40626687
- Backeljauw PF, et al. Challenges in the care of individuals with severe primary insulin-like growth factor-I deficiency (SPIGFD): an international, multi-stakeholder perspective. Orphanet Journal of Rare Diseases 2023 · PMID 37805563
- LeRoith D, et al. Insulin-like growth factors: Ligands, binding proteins, and receptors. Molecular Metabolism 2021 · PMID 33962049
- Fintini D, et al. Profile of mecasermin for the long-term treatment of growth failure in children and adolescents with severe primary IGF-1 deficiency. Therapeutics and Clinical Risk Management 2009 · PMID 19707272
- Vilmann L, et al. Bioactive Insulin-like Growth Factor (IGF)-I Concentrations in Children on Growth Hormone Therapy. Journal of Clinical Endocrinology and Metabolism 2025 · PMID 41083160
Increlex — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- This is IGF-1 itself, not something that asks your body for IGF-1. Every other compound on the GH axis in this Vault works by persuading the pituitary to pulse and the liver to respond, and the liver's regulatory step is also a brake. Delivering the finished hormone removes that brake, which is why the risk profile here is sharper than anything upstream of it.
- Hypoglycemia is the dose-limiting risk, and it is not a rare one. IGF-1 has real activity at the insulin receptor. In the registration trials 42% of patients had hypoglycemia and five had severe episodes involving seizure or loss of consciousness. That is one of the very few numbers on any card in this Vault that comes from a label rather than from a mechanism.
- IGF-1 is a growth signal for lymphoid tissue: tonsillar and adenoidal hypertrophy is documented at 15%, and it progresses to snoring, obstructive sleep apnea and middle-ear effusion.
- Intracranial hypertension — headache with nausea and visual change — was reported in roughly 4%.
- Where growth plates are still open, the label carries slipped capital femoral epiphysis and progression of scoliosis. Those are pediatric findings and they are the reason a limp or new hip or knee pain is treated as urgent rather than as a training niggle.
- The proliferation question that runs through the whole GH axis is sharper here for the same reason everything else is: this is the growth signal itself, and growth signals do not distinguish between tissue you want and tissue you do not.
What has actually been reported
- Unusually for this section of the Vault, all of the above is observed rather than predicted. Increlex is an approved drug with a real label and real trial numbers behind every figure quoted here.
- What is NOT observed is any of it in healthy adults using it for body composition. Every number comes from children with severe primary IGF-1 deficiency — a population whose IGF-1 started near zero. That is not the population reading this page.
How to reduce the risk
Same mechanism as the prediction.
- Eat with it — within about twenty minutes either side of a meal or snack. This is the label instruction and it is the single most important line on this card. It is also the exact opposite of how the GH secretagogues on neighboring pages are timed, which are usually taken fasted to avoid blunting the pulse. Carrying the fasted habit across from the compound next to it on the shelf is the realistic way somebody gets hurt with this drug.
- Do not drive or train hard for two to three hours after a dose until you know your own response.
- Learn what your hypoglycemia feels like — shaking, sweating, confusion, sudden hunger — and keep fast carbohydrate within reach of where you inject. The severe cases in the trials were seizures, and a seizure is what an untreated hypo eventually becomes.
- New snoring or daytime sleepiness is the lymphoid arm reporting in, not a coincidence. Persistent headache with nausea or visual change is the intracranial arm, and it needs eyes looked at rather than a dose adjustment.
What it does to your bloodwork
A fact about the assay.
- Fasting glucose and HbA1c before you start, because the dose-limiting risk is a glucose risk and you want the comparison.
- IGF-1 itself — and note that an IGF-1 drawn while running this is measuring the injection, not your axis. If you want a real baseline, draw it first.
- A funduscopic examination is the label's recommendation at initiation and periodically, which is unusual enough to be worth taking literally.
Don't run this if
- Active malignancy or any history of it. This is a labeled contraindication, not a caution.
- Closed epiphyses, where the purpose is growth — also a labeled contraindication.
- The formulation contains benzyl alcohol, which carries serious and fatal reactions in infants and is a reason the pediatric labeling is specific about who may receive it.
The honest unknown
- What direct IGF-1 does to an adult whose GH axis is already intact and whose IGF-1 is already normal. The entire evidence base is replacement in deficiency; the entire off-label use is addition on top of sufficiency. Those are different questions and only one has been asked.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Increlex — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Increlex moves on your bloodwork
Expected direction, not a measured one.
- IGF-1 (Insulin-like Growth Factor 1) — ↑ expected to rise
This is the point. IGF-1 rising is the compound doing its job — it is the stable downstream readout of a GH pulse.
What to do: Test it before you start and again at 6–8 weeks. It is the only number that tells you whether the product was real and the dose was enough. - Growth Hormone, Serum — ✕ unreliable here
A random GH level is close to meaningless here. GH is secreted in pulses during deep sleep and sits undetectable between them, so a daytime draw catches a trough almost every time — including when the compound is working perfectly.
What to do: Do not use GH to judge a secretagogue. Read IGF-1 instead. - Fasting Insulin — ↑ expected to rise
GH is a counter-regulatory hormone: it opposes insulin. Fasting insulin and glucose drifting up is the predicted trade-off, not a surprise.
What to do: Check fasting insulin and HbA1c at baseline and again at 8–12 weeks. This is the marker that decides whether you keep running it. - HbA1c (Hemoglobin A1c) — ↑ expected to rise
Same mechanism, longer window — a slow drift rather than a jump.
What to do: Pair it with fasting insulin; either alone can mislead. - Free T4 (Thyroxine) — ↓ expected to fall
GH accelerates the peripheral conversion of T4 to T3, so free T4 can fall while free T3 holds or rises. Read alone it looks like new hypothyroidism, and it usually isn't.
What to do: Run a full thyroid panel rather than TSH alone before concluding anything.
Everything above follows from one fact: these raise GH and therefore IGF-1. Nothing here needs a trial of the specific molecule.
- Dose range and how to work up to it
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Increlex in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Increlex
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| IGF-1 (Insulin-like Growth Factor 1) | The number that actually tracks your GH exposure — dose by this, not by feel |
| Fasting Insulin | GH raises insulin resistance; this moves before glucose does |
| HbA1c (Hemoglobin A1c) | The slower confirmation that the insulin change is real |
| Comprehensive Metabolic Panel (CMP) | Fasting glucose, and liver and kidney at baseline |
The “Running GH Peptides or MK-677” panel covers these in one order — 9 markers, $132.30 with the discount applied.
Check results you already have → · All 103 markers A–Z
Increlex — frequently asked questions
What is Increlex?
Increlex (mecasermin — recombinant human IGF-1) is a gh & growth research compound. Recombinant human IGF-1 itself, not a secretagogue. Everything upstream — GHRH analogs, ghrelin mimetics, growth hormone — exists to raise IGF-1. This is the endpoint delivered directly, which removes the liver's regulatory step and the negative feedback that comes with it.
Where can I find Increlex dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Increlex protocol are available to members inside Skool. This public page covers what Increlex is, how it works and the evidence.
What is the half-life of Increlex?
Increlex has an approximate half-life of ~5.8 hrs, which is part of what determines how often it's dosed.
What's the evidence behind Increlex?
Current evidence level: FDA-approved (severe primary IGF-1 deficiency); human. Increlex is offered for research purposes only and is not an approved medicine.
What Increlex is used for
Increlex appears under 1 goal in the goal router.
Related GH & Growth compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.