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Somapacitan

A once-weekly growth hormone analogue that binds reversibly to albumin to stretch a daily injection into a weekly one, approved for both adult and paediatric growth hormone deficiency.

Also known as Somapacitan-beco, Long-acting growth hormone, Sogroya, NNC0195-0092

Approved drug — Licensed by a major regulator for human use, with phase-3 trial data behind it.

Approved by the FDA in 2020 for adult GH deficiency and later extended to paediatric GH deficiency, on the strength of the REAL phase 3 programme showing non-inferiority to daily somatropin on body composition and growth velocity respectively. The efficacy question here is essentially settled; the open question is only long-term safety of weekly versus daily GH exposure patterns.

How it works

Somapacitan is human GH with a single amino-acid substitution at position 101 carrying an albumin-binding fatty-acid side chain attached via a hydrophilic linker. The non-covalent albumin association slows renal clearance and receptor-mediated elimination, giving a profile that supports once-weekly dosing while preserving normal GH receptor agonism and JAK2/STAT5 signalling. Because free drug concentration is buffered by the albumin reservoir, peak-to-trough IGF-1 swings across the week are smaller than the once-weekly dosing interval would suggest, though IGF-1 does still peak around days 2 to 4 - which is why the timing of IGF-1 sampling matters when titrating.

Targets: Growth hormone receptor (GHR), Serum albumin, JAK2/STAT5 pathway, Hepatic IGF-1 production

Dosing

ProtocolDoseFrequencyRoute
Adult GH deficiency (label)Same day each week, any time of day, rotating sites.1 mg – 2 mgonce weeklysubcutaneous
Adult titration ceilingWeekly.2 mg – 8 mgonce weeklysubcutaneous
Paediatric GH deficiency (label)Weekly, same day.—once weeklysubcutaneous
  • · Start 1.5 mg weekly for adults 18 to 60, 1.0 mg for over 60, and 2.0 mg for women on oral oestrogen. Titrate by 0.5 to 1.5 mg every 2 to 4 weeks against IGF-1.
  • · The maximum labelled adult dose is 8 mg once weekly. Most people settle well below that.
  • · 0.16 mg per kg body weight once weekly.

Titration

Titrate against IGF-1 SDS measured 3 to 4 days after the dose, adjusting every 2 to 4 weeks. Sampling at a different point in the week gives a misleading number.

Cycling

This is a chronic replacement therapy, not a cycle. Treatment continues as long as the deficiency and the benefit persist, with periodic reassessment.

Work out your exact syringe units →

Pharmacology

Half-life
Roughly two to three days, supporting once-weekly dosing; it varies with dose and body weight.
Onset
IGF-1 rises within the first week; body-composition and quality-of-life effects accrue over 3 to 6 months.
Routes
subcutaneous
Molecule
Recombinant human GH analogue with a non-covalent albumin-binding side chain
Sequence length
191 amino acids
Molecular weight
23305 Da

Handling

Diluent
Not applicable - supplied as a ready-to-use prefilled pen
Vial sizes
5, 10, 15 mg
Lyophilised
Not applicable; store unused pens refrigerated at 2 to 8 degrees C.
Reconstituted
An in-use pen may be kept refrigerated for up to 6 weeks, or at room temperature for a shorter labelled period - check the carton for the specific strength.
Light sensitive
Yes — keep it out of the light

Mixing

Sogroya comes as a prefilled multi-dose pen in 5, 10 and 15 mg strengths. Nothing to mix.

Side effects

  • commonPeripheral oedema— Class GH effect, dose-related.
  • commonArthralgia and musculoskeletal stiffness
  • commonHeadache
  • commonInjection-site reactions
  • uncommonAdrenal insufficiency unmasked— GH reduces cortisol regeneration via 11-beta-HSD-1 and can reveal previously compensated adrenal insufficiency - a labelled warning.
  • uncommonIncreased fasting glucose
  • uncommonAnti-drug antibody formation— Detected in trials without clear loss of efficacy.

Do not use if

  • Active malignancy.
  • Acute critical illness following open heart or abdominal surgery, multiple accidental trauma or acute respiratory failure.
  • Active proliferative or severe non-proliferative diabetic retinopathy.
  • Closed epiphyses in children being treated for growth.
  • Known hypersensitivity to somapacitan or excipients.

Combining it

  • conflictOral oestrogen — Reduces the IGF-1 response; women on oral oestrogen start at a higher dose per the label.
  • cautionGlucocorticoids — Cortisone and prednisone requirements may rise because GH suppresses 11-beta-HSD-1.
  • cautioninsulin — Insulin and oral hypoglycaemic requirements may increase.
  • redundantsomatropin — Same receptor, same purpose. Somapacitan replaces daily GH; it does not add to it.

What to monitor

  • · IGF-1 SDS measured 3 to 4 days after a dose, at baseline and every 2 to 4 weeks during titration, then every 6 to 12 months.
  • · Fasting glucose and HbA1c.
  • · Cortisol status where adrenal insufficiency is possible.
  • · Thyroid function.
  • · In children, growth velocity and bone age.

Legal status

FDA and EMA approved, prescription-only. Prohibited in sport under WADA S2.

References

  • Johannsson et al. 2020 JCEM, REAL 1 phase 3 trial of weekly somapacitan in adult GH deficiency (trial)
  • Sogroya (somapacitan-beco) FDA prescribing information (label)

Mechanism in depth

Somapacitan solves the same problem as CJC-1295's drug affinity complex by a different and gentler route. Instead of forming a permanent covalent bond to albumin cysteine-34, it carries a fatty-acid side chain that binds albumin's fatty-acid pockets reversibly. That creates a circulating depot in dynamic equilibrium with free drug: albumin-bound somapacitan is protected from renal filtration and from receptor-mediated clearance, and free drug is continuously replenished from the reservoir as it is consumed. The consequence visible in the label is a strikingly small apparent volume of distribution - 14.6 L, essentially the plasma volume plus a little - and greater than 99 percent protein binding. Receptor pharmacology is conventional somatropin: site 1 then site 2 binding, receptor dimer realignment, JAK2 transphosphorylation, STAT5b, hepatic IGF-1. Petersen's tissue distribution study addressed the question that matters for any modified long-acting GH: does the bulky modification stop the molecule reaching target tissues? They demonstrated prolonged biodistribution and receptor activation, which is reassuring, though it is a preclinical imaging study rather than a human one. The practical detail that separates competent use from incompetent use is IGF-1 sampling timing. Because the buffering effect of the albumin reservoir smooths but does not abolish the weekly cycle, IGF-1 peaks a few days after the dose - the label specifies drawing IGF-1 samples 3 to 4 days after the prior dose during titration. Sampling on day 7 gives a trough that reads as under-replacement and invites a dose increase that is not warranted; sampling on day 1 gives the opposite. Steady state arrives after one to two weeks of weekly dosing.

What usually goes wrong

IGF-1 sampling at the wrong point in the week is the characteristic error with every long-acting GH, and it produces confidently wrong dosing. A trough sample on day 7 reads low, prompts an increase, and the patient ends up over-replaced with the arthralgia and oedema that follow. Draw on day 3 or 4. The second issue is the in-use pen period: refrigerated for up to six weeks, or a shorter labelled period at room temperature depending on strength, and the specific numbers differ between the 5, 10 and 15 mg pens. The third is assuming that once-weekly means the pharmacology is forgiving; a mistimed or doubled dose is a week-long problem. Adrenal insufficiency unmasking applies here as it does to every GH product, and in a hypopituitary population that is not a theoretical risk.

Titration ladder

  1. 1.5 mgStarting dose, adults 18 to 60 — 1.5 mg once weekly, same day each week, any time of day, rotating sites.
  2. 1 mgStarting dose, adults over 60 — 1.0 mg once weekly. Older adults are more sensitive to GH side effects and the label reflects that.
  3. 2 mgStarting dose, women on oral oestrogen — 2.0 mg once weekly. Oral oestrogen blunts the hepatic IGF-1 response through a first-pass effect, so the same dose produces less IGF-1. Transdermal oestrogen does not do this.
  4. 500 mcgTitration, every 2 to 4 weeks — Increase by 0.5 to 1.5 mg per step, guided by IGF-1 SDS drawn 3 to 4 days after the prior dose. The doseMcg here is the increment, not a total dose.
  5. 8 mgCeiling — 8 mg once weekly is the maximum labelled adult dose. Paediatric dosing is entirely different: 0.16 mg per kg once weekly.

Bloodwork worth running

MarkerWhenWhy it matters
IGF-1 standard deviation scoreDraw 3 to 4 days after the prior dose - this is a labelled instruction, not a refinement. Baseline, then every 2 to 4 weeks during titration, then every 6 to 12 months.The titration target, and the one place where somapacitan demands more discipline than daily GH. Sampling at the wrong point in the weekly cycle produces a number that is simply wrong, and dosing decisions made on it will be wrong too.Act if: Keep IGF-1 SDS within the normal range. Titrate by 0.5 to 1.5 mg every 2 to 4 weeks; the maximum labelled adult dose is 8 mg weekly and most people settle well below it.
Fasting glucose and HbA1cBaseline and every 6 to 12 months.Class effect. Reassuringly, a dedicated analysis found no adverse effect of weekly somapacitan on glucose metabolism in adults with GH deficiency, which is a better result than the GH class average.Act if: A rise into the prediabetic range warrants a dose review, though it is less expected here than with daily GH at equivalent IGF-1.
Morning cortisol and adrenal statusBaseline where adrenal insufficiency is possible; urgently on new fatigue, nausea, dizziness or hypotension.The 11-beta-HSD-1 effect applies to every GH product and carries a labelled warning. In a hypopituitary population this is the marker most likely to matter acutely.Act if: Low or borderline cortisol needs formal assessment before continuing.
Free T4 and TSHBaseline and every 6 to 12 months.GH increases T4 to T3 conversion and can unmask central hypothyroidism, which is common in the hypopituitary population somapacitan is prescribed for.Act if: Falling free T4 needs replacement adjusted.
Anti-drug antibodiesOnly on unexplained loss of response.Detected in trials without clear loss of efficacy, but relevant if a previously responding patient stops responding.Act if: Unexplained falling IGF-1 on a stable dose is the trigger to ask about immunogenicity.

Pharmacokinetics

Tmax
14 h
Volume of distribution
14.6 L
Protein binding
99%
Time to steady state
10.5 days
Crosses blood-brain barrier
no
Accumulates
Yes — doses stack before steady state
Metabolism
Reversible, non-covalent albumin binding via a fatty-acid side chain attached to a substitution at position 101 through a hydrophilic linker. Greater than 99 percent plasma protein bound. Ultimately proteolytic catabolism.
Elimination
Approximately 81 percent of the dose is excreted in urine and approximately 13 percent in faeces, per the label.

Receptor targets

  • Growth hormone receptor (GHR) — Conventional GH receptor agonism, retained despite the side-chain modification

    Receptor dimer realignment, JAK2/STAT5b signalling, hepatic IGF-1 transcription. Pharmacologically it is growth hormone.

  • Serum albumin fatty-acid binding sites — Non-covalent and reversible; greater than 99 percent plasma protein binding

    Creates a circulating depot that protects the drug from renal and receptor-mediated clearance and buffers free drug concentration across the week. Not a pharmacological target - the delivery mechanism.

  • 11-beta-hydroxysteroid dehydrogenase type 1 — Inhibited, as with all GH

    Reduced cortisol regeneration, with the same capacity to unmask compensated adrenal insufficiency that carries a labelled warning across the GH class.

Trials

  • REAL 1 - Johannsson et al., once-weekly somapacitan versus daily growth hormone in adults with GH deficiency 3 · 34 weeks · 2020

    Change in truncal fat percentage. Once-weekly somapacitan was effective and well tolerated in adults with GH deficiency, supporting the weekly dosing interval against daily somatropin.

  • Takahashi et al., glucose metabolism analysis of weekly somapacitan in adults with GH deficiency 3 analysis · 2023

    Weekly somapacitan had no adverse effects on glucose metabolism in adults with growth hormone deficiency - a specific and useful negative finding given how routinely glucose deterioration is expected across this class.

What to expect, and when

Peak concentration 4 to 24 hours after the dose, half-life 2 to 3 days, steady state after one to two weeks of weekly dosing. IGF-1 rises within the first week and peaks around days 2 to 4 of each weekly cycle. Body composition and quality-of-life effects accrue over three to six months, which is the timeframe the phase 3 trial measured. In children, growth velocity is assessed at 12 months.

Stacking and comparisons

This is replacement therapy and there is nothing sensible to stack it with. It substitutes for daily somatropin rather than adding to it, and combining it with any GH secretagogue is pointless because exogenous GH suppresses the pituitary. The interactions that matter are the same endocrine ones that apply to all GH: oral oestrogen reduces the IGF-1 response and is explicitly reflected in a higher starting dose in the label; glucocorticoid requirements may rise because GH suppresses 11-beta-HSD-1; insulin and oral hypoglycaemic requirements may increase, though the dedicated glucose analysis found weekly somapacitan unusually benign in this respect.

Against daily somatropin: the phase 3 programme established non-inferiority, so the choice is about adherence and preference rather than efficacy. One injection a week instead of seven is a genuine quality-of-life difference in a lifelong therapy. Against lonapegsomatropin: lonapegsomatropin releases unmodified somatropin from an inert carrier, so the molecule reaching the receptor is ordinary GH and tissue distribution is not in question; somapacitan is a permanently modified molecule, which is why the Petersen distribution work exists. Both are approved and both work. Against somatrogon: somatrogon is paediatric-only in most jurisdictions and has notably more injection-site reactions; somapacitan has both adult and paediatric indications. Against CJC-1295 with DAC: superficially similar - both use albumin to extend half-life - but somapacitan is GH acting at the GH receptor with a phase 3 programme, and CJC-1295 is a GHRH analogue acting on the pituitary with one phase 1/2 study and no manufacturing oversight.

Rough cost

$2000–$4500/month. US cash pricing for Sogroya prefilled pens runs into the thousands of dollars a month and is essentially only accessible through insurance. This is a prescription biologic for a diagnosed indication, not a grey-market product, and there is no meaningful off-label supply. Figures are approximate.

Genuinely uncertain

  • The exact identity of the position-101 substitution and the structure of the linker and fatty-acid side chain were not resolved from a primary source in this session, so the sequence entry is flagged unverified. The Core record's molecular weight of 23305.0 was likewise not confirmed.
  • Absolute bioavailability is not stated in the label.
  • No apparent clearance value is published.
  • The 14 hour tmax entered here is the midpoint of the labelled 4 to 24 hour adult range, not a reported point estimate. The 10.5 day steady-state figure is the midpoint of the labelled 1 to 2 week range.
  • Long-term safety of weekly versus daily GH exposure patterns remains the open question for this whole product category, and registry follow-up is ongoing rather than complete.
  • The Petersen tissue distribution work is preclinical imaging; human target-tissue penetration has not been directly measured.

Papers