Octreotide
The original somatostatin analogue, approved since 1988 for acromegaly, carcinoid syndrome and VIPoma. Extensively characterised.
Growth Hormone
Pasireotide
A somatostatin analogue with broad receptor coverage, approved for Cushing's disease and for acromegaly not controlled on other analogues. Hyperglycaemia is its defining limitation.
Overview
Older somatostatin analogues mostly hit one receptor subtype. Pasireotide binds four of the five, and in particular it binds SSTR5 much more strongly. That extra coverage is what lets it suppress ACTH in Cushing's disease, which octreotide cannot do. The same broad binding is why it causes high blood sugar far more often — SSTR5 is heavily involved in insulin release.
A cyclohexapeptide with high affinity for SSTR1, 2, 3 and 5, notably around 40-fold greater SSTR5 affinity than octreotide. SSTR5 predominance on corticotroph adenomas underlies the ACTH-lowering effect in Cushing's disease. The same SSTR5 activity on pancreatic beta cells markedly suppresses insulin and incretin secretion, producing hyperglycaemia in a majority of treated patients — reported in roughly 70% in the pivotal Cushing's trial. Available as twice-daily subcutaneous and monthly intramuscular LAR formulations.
Research areas
Cushing's diseaseAcromegalyPituitary adenoma
Dosing reported in the literature
Every protocol below is reproduced from a published study or approved labelling, with its source named. These are records of what was studied — not recommendations, and not a suggestion that any of them is appropriate for any person.
| Protocol as reported | Source |
|---|---|
| 0.6 mg or 0.9 mg subcutaneously twice daily in Cushing's disease | Colao et al., New England Journal of Medicine 2012 |
| 40 mg or 60 mg intramuscularly every 28 days in acromegaly inadequately controlled on first-generation analogues | PAOLA, The Lancet Diabetes & Endocrinology 2014 |
Trial status
Phase 3 completed in both Cushing's disease and acromegaly.
Reported safety signals
- Hyperglycaemia occurs in the large majority of patients and frequently requires antidiabetic treatment. This is the single most important consideration with this drug.
- Gallstones, diarrhoea and nausea occur as with other somatostatin analogues.
- QT prolongation has been observed.
- Hypocortisolism can develop as ACTH is suppressed; monitoring is required.
Common questions
Why does pasireotide raise blood sugar so much?
Its high affinity for the SSTR5 receptor is exactly what makes it work in Cushing's disease, and SSTR5 is also heavily expressed on the beta cells that release insulin. Suppressing insulin and the incretin response is an unavoidable consequence of the receptor profile, not a rare side effect.
Primary sources
Medical disclaimer
This page is for informational and research purposes only. Nothing here constitutes medical advice. The compounds discussed are research chemicals. Consult a qualified clinician before starting any protocol.
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