Why does pasireotide cause high blood sugar?

Its broad somatostatin-receptor activity suppresses insulin and the incretin hormone GLP-1, which raises blood glucose and can trigger or worsen diabetes in a large share of patients.

Is pasireotide more effective than older somatostatin analogs?

In acromegaly it showed superior biochemical control versus octreotide and benefit in patients inadequately controlled on octreotide or lanreotide, but at the cost of more hyperglycaemia.

What monitoring does pasireotide require?

Blood glucose before and during treatment, plus checks of liver enzymes, ECG/QT interval, gallbladder status, and cortisol levels.

EMA-approvedaka Signifor

Pasireotide — Complete Research Guide (2026)

Q: How is pasireotide administered?

Either as a twice-daily subcutaneous injection or as a once-monthly long-acting intramuscular depot, prescribed and monitored by an endocrinologist.

Last updated 2026-06-30

TL;DR

Pasireotide (also known as Signifor) is a peptide catalogued under Hormones & Metabolic (Multi-receptor somatostatin analog). It is described as: SSTR1/2/3/5. Documented context: Cushing disease; acromegaly. Neutral reference entry; EU status: EU-approved prescription medicine.

What is Pasireotide?

Pasireotide (marketed as Signifor and Signifor LAR) is a multi-receptor-targeted somatostatin analog approved by the FDA and EMA for Cushing's disease in patients not candidates for or not cured by surgery, and in its long-acting form for acromegaly inadequately controlled by other therapy.

The evidence level is high: approvals are based on pivotal phase 3 randomized human trials including a 12-month Cushing's disease study and the PAOLA acromegaly trial.

How does Pasireotide work?

Pasireotide binds four of the five somatostatin receptor subtypes (1, 2, 3, and 5), with especially high affinity for subtype 5, giving broader receptor coverage than octreotide or lanreotide.

This suppresses ACTH secretion in Cushing's disease and growth hormone/IGF-1 in acromegaly, but the same receptor activity also suppresses insulin and incretin (GLP-1) release, which drives hyperglycaemia.

What does the research say about Pasireotide?

In Cushing's disease, pasireotide significantly reduced urinary free cortisol and normalized it in a subset of patients over 12 months. ^[1]
In acromegaly inadequately controlled on first-generation analogs, switching to pasireotide LAR improved biochemical control versus continued octreotide or lanreotide (PAOLA). ^[2]
Head-to-head, pasireotide achieved superior biochemical control of acromegaly compared with octreotide. ^[3]

Clinical research & studies

The references below are the primary sources cited throughout this guide. Each links directly to PubMed or the regulator. Where evidence is preclinical (animal or in-vitro), that is stated rather than implied.

[1] A 12-month phase 3 study of pasireotide in Cushing's disease — Colao A et al., New England Journal of Medicine 2012. (Phase 3 randomized controlled trial)
[2] Pasireotide versus continued treatment with octreotide or lanreotide in patients with inadequately controlled acromegaly (PAOLA): a randomised, phase 3 trial — Gadelha MR et al., Lancet Diabetes and Endocrinology 2014. (Phase 3 randomized controlled trial (PAOLA))
[3] Pasireotide versus octreotide in acromegaly: a head-to-head superiority study — Colao A et al., Journal of Clinical Endocrinology and Metabolism 2014. (Randomized controlled superiority trial)
[4] Long-acting pasireotide improves clinical signs and quality of life in Cushing's disease: results from a phase III study — Lacroix A et al., Journal of Endocrinological Investigation 2020. (Phase 3 study analysis)
[5] Risk factors and management of pasireotide-associated hyperglycemia in acromegaly — Gadelha MR et al., Endocrine Connections 2020. (Review/analysis of trial data)
[6] Pasireotide for acromegaly: long-term outcomes from an extension to the Phase III PAOLA study — Colao A et al., European Journal of Endocrinology 2020. (Phase 3 extension study)

Dosing context

This is not medical advice or a usage recommendation. Dosing figures are reported research context only, cited from the published literature.

This is context only and not dosing advice: pasireotide is available as a twice-daily subcutaneous injection (Signifor) and as a once-monthly long-acting intramuscular depot (Signifor LAR), with dose selected by an endocrinologist.

Because of the hyperglycaemia risk, glucose status is assessed before starting and monitored throughout treatment.

Side effects & safety profile

The signature and clinically important adverse effect of pasireotide is hyperglycaemia and new or worsening diabetes, caused by suppression of insulin and GLP-1 secretion; it occurs in a large proportion of patients and often requires glucose monitoring and antidiabetic treatment.

Other risks include gallstones, diarrhoea and other gastrointestinal effects, QT-interval prolongation, elevated liver enzymes, and hypocortisolism from over-suppression.

It is a specialist-only prescription drug requiring baseline and ongoing glucose and cardiac monitoring.

Stacking & combinations

In practice it may be combined with glucose-lowering agents to manage its hyperglycaemia, or with other pituitary-directed therapies under specialist care, rather than being combined for enhancement purposes.

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Frequently asked questions

It is an approved prescription treatment for Cushing's disease when surgery is not an option or has failed, and its long-acting form is approved for acromegaly not adequately controlled by other therapies.

References

[1] A 12-month phase 3 study of pasireotide in Cushing's disease — Colao A et al., New England Journal of Medicine 2012. PMID: 22397653. View sourceStudy: Phase 3 randomized controlled trialPasireotide lowered urinary free cortisol and normalized it in a subset of Cushing's disease patients, but hyperglycaemia-related events were frequent.
[2] Pasireotide versus continued treatment with octreotide or lanreotide in patients with inadequately controlled acromegaly (PAOLA): a randomised, phase 3 trial — Gadelha MR et al., Lancet Diabetes and Endocrinology 2014. PMID: 25260838. View sourceStudy: Phase 3 randomized controlled trial (PAOLA)Pasireotide LAR achieved biochemical control in more inadequately-controlled acromegaly patients than continued octreotide or lanreotide, with more hyperglycaemia.
[3] Pasireotide versus octreotide in acromegaly: a head-to-head superiority study — Colao A et al., Journal of Clinical Endocrinology and Metabolism 2014. PMID: 24423324. View sourceStudy: Randomized controlled superiority trialPasireotide provided superior biochemical control of acromegaly versus octreotide but caused more hyperglycaemia.
[4] Long-acting pasireotide improves clinical signs and quality of life in Cushing's disease: results from a phase III study — Lacroix A et al., Journal of Endocrinological Investigation 2020. PMID: 32385851. View sourceStudy: Phase 3 study analysisLong-acting pasireotide improved clinical signs and quality-of-life measures in Cushing's disease.
[5] Risk factors and management of pasireotide-associated hyperglycemia in acromegaly — Gadelha MR et al., Endocrine Connections 2020. PMID: 33434154. View sourceStudy: Review/analysis of trial dataCharacterizes predictors of pasireotide-associated hyperglycaemia and outlines monitoring and management strategies.
[6] Pasireotide for acromegaly: long-term outcomes from an extension to the Phase III PAOLA study — Colao A et al., European Journal of Endocrinology 2020. PMID: 32217809. View sourceStudy: Phase 3 extension studyExtended treatment maintained biochemical control in acromegaly, with hyperglycaemia remaining the key adverse effect.

This article is for educational and research purposes only. Peptides discussed here are not approved for human consumption by the FDA, EMA, or equivalent regulators outside of specific clinical contexts. Always consult a licensed medical professional before any therapeutic use.