Pasireotide is an active pharmaceutical ingredient in the Somatostatin and Analogues group (H01CB). The information below is compiled per regulator from the product labels on record, with direct links to the original documents.
GBOfficial regulatory label· revised May 1, 2026[1]
Treatment of adult patients with Cushing’s disease for whom surgery is not an option or for whom surgery has failed.
How to take
GB
CACanada· Health Canada
8 products
Side effects & warnings
CAOfficial regulatory label· Warnings and precautions· revised May 30, 2025[2]
– Monitoring and Laboratory Tests). Pancreatic enzymes Acromegaly In the drug-naïve Study C2305, asymptomatic elevations in lipase and alpha amylase were observed in 31% and 24% of patients. In Study C2402 evaluating patients previously treated with somatostatin analogs, asymptomatic elevations in alpha amylase were reported in 10% in the 40 mg arm and in 5% in the 60 mg arm.
Asymptomatic elevations in lipase were reported only in the 40 mg arm in 2% of patients. 9 per 100 PYE in both phase 3 studies and across all doses. 7%) patients, respectively. 7%) patient in the 30 mg group. There were no grade 4 events reported.
3%) in the 10 mg and 30 mg dose groups, respectively) (see 7 WARNINGS AND PRECAUTIONS – Monitoring and Laboratory Tests). Pancreatitis is a potential adverse reaction associated with the use of somatostatin analogs due to the association between cholelithiasis and acute pancreatitis.
EUEuropean Union· EMA
1 product
Uses
EUOfficial regulatory label· revised December 18, 2024[3]
Treatment of adult patients with Cushing’s disease for whom surgery is not an option or for whom surgery has failed.
How to take
EU
Drug interactions
Known interactions involving Pasireotide. Select one for details. This list is informational and not a complete interaction checker.
Showing 240 of 332. Type above to find a specific drug.
Interaction data compiled from DDInter (academic, CC-BY). Severity classification only - this is not a complete interaction checker and not medical advice.
[1]MHRA (UK) · PLGB152660032 · revised May 1, 2026
[2]Health Canada (DPD) · 02437252 · revised May 30, 2025
[3]European Medicines Agency · EMEA/H/C/002052 · revised December 18, 2024
Information on this page is compiled from public regulatory records. Drugvu is not affiliated with any regulator or pharmaceutical manufacturer. This is not medical advice. Always consult a qualified healthcare professional.
6 mg pasireotide by subcutaneous injection twice a day. Two months after the start of Signifor therapy, patients should be evaluated for clinical benefit. Patients who experience a significant reduction in urinary free cortisol (UFC) levels should continue to receive Signifor for as long as benefit is derived.
6 mg dose is well tolerated by the patient. Patients who have not responded to Signifor after two months of treatment should be considered for discontinuation. Management of suspected adverse reactions at any time during the treatment may require temporary dose reduction of Signifor.
3 mg twice a day is suggested. If a dose of Signifor is missed, the next injection should be administered at the scheduled time. Doses should not be doubled to make up for a missed dose. Switch from intramuscular to subcutaneous formulation There are no clinical data available on switching from the intramuscular to the subcutaneous pasireotide formulation.
6 mg pasireotide twice a day. The patient should be monitored for response and tolerability and further dose adjustments may be needed. Special populations Paediatric population The safety and efficacy of Signifor in children and adolescents aged 0 to 18 years have not been established.
No data are available. 2). 2). Hepatic impairment Dose adjustment is not required in patients with mildly impaired hepatic function (Child Pugh A). 2). 6 mg twice a day. 4). Method of administration Signifor is to be administered subcutaneously by self injection.
Patients should receive instructions from the physician or a healthcare professional on how to inject Signifor subcutaneously. Use of the same injection site for two consecutive injections is not recommended. Sites showing signs of inflammation or irritation should be avoided.
Preferred injection sites for subcutaneous injections are the top of the thighs and the abdomen (excluding the navel or waistline). 6.
This is not medical advice. Consult a qualified healthcare professional.
Side effects & warnings
GBOfficial regulatory label· Adverse reactions· revised May 1, 2026[1]
Summary of the safety profile A total of 201 Cushing’s disease patients received Signifor in phase II and III studies. The safety profile of Signifor was consistent with the somatostatin analogue class, except for the occurrence of hypocortisolism and degree of hyperglycaemia.
The data described below reflect exposure of 162 Cushing’s disease patients to Signifor in the phase III study. 9 mg Signifor. 8%) were female. 3%) patients had persistent or recurrent Cushing’s disease and few (≤5%) in either treatment group had received previous pituitary irradiation.
0% of patients having at least six months’ exposure. 4% of patients. 5% of patients. Grade 3 and 4 adverse reactions were mostly related to hyperglycaemia. The most common adverse reactions (incidence ≥10%) were diarrhoea, nausea, abdominal pain, cholelithiasis, injection site reactions, hyperglycaemia, diabetes mellitus, fatigue and glycosylated haemoglobin increased.
Tabulated list of adverse reactions Adverse reactions reported up to the cut-off date of the analysis are presented in Table 1. Adverse reactions are listed according to MedDRA primary system organ class. Within each system organ class, adverse reactions are ranked by frequency.
Within each frequency grouping, adverse reactions are presented in the order of decreasing seriousness.
Frequencies were defined as follows:
Very common (≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); not known (cannot be estimated from the available data). 2% of patients) in the phase III study in Cushing’s disease patients. e. e. e. 30% at month 6). Mean fasting plasma glucose levels commonly increased within the first month of treatment, with decreases and stabilisation observed in subsequent months.
Fasting plasma glucose and HbA1c values generally decreased over the 28 days following pasireotide discontinuation but remained above baseline values. Long-term follow-up data are not available. Patients with baseline HbA1c ≥7% or who were taking antidiabetic medicinal products prior to randomisation tended to have higher mean changes in fasting plasma glucose and HbA1c relative to other patients.
5%) patients, respectively. One case of ketosis and one case of ketoacidosis have been reported during compassionate use of Signifor. 4). Gastrointestinal disorders Gastrointestinal disorders were frequently reported with Signifor. These reactions were usually of low grade, required no intervention and improved with continued treatment.
6% of patients enrolled in the phase III study in Cushing’s disease. Injection site reactions were also reported in clinical studies in other populations. The reactions were most frequently reported as local pain, erythema, haematoma, haemorrhage and pruritus.
These reactions resolved spontaneously and required no intervention. Liver enzymes Transient elevations in liver enzymes have been reported with the use of somatostatin analogues and were also observed in patients receiving pasireotide in clinical studies.
The elevations were mostly asymptomatic, of low grade and reversible with continued treatment. Rare cases of concurrent elevations in ALT greater than 3 x ULN and bilirubin greater than 2 x ULN have been observed. All cases of concurrent elevations were identified within ten days of initiation of treatment with Signifor.
The patients recovered without clinical sequelae and liver function test results […]
GBOfficial regulatory label· Warnings and precautions· revised May 1, 2026[1]
Glucose metabolism Alterations in blood glucose levels have been frequently reported in healthy volunteers and patients treated with pasireotide. 8). The degree of hyperglycaemia appeared to be higher in patients with pre-diabetic conditions or established diabetes mellitus.
8). 9 mg twice daily. e. glucagon-like peptide-1 [GLP-1] and glucose-dependent insulinotropic polypeptide [GIP]). Glycaemic status (fasting plasma glucose/haemoglobin A1c [FPG/HbA1c]) should be assessed prior to starting treatment with pasireotide.
FPG/HbA1c monitoring during treatment should follow established guidelines. Self monitoring of blood glucose and/or FPG assessments should be done weekly for the first two to three months and periodically thereafter, as clinically appropriate, as well as over the first two to four weeks after any dose increase.
In addition, monitoring of FPG 4 weeks and HbA1c 3 months after the end of the treatment should be performed. If hyperglycaemia develops in a patient being treated with Signifor, the initiation or adjustment of antidiabetic treatment is recommended, following the established treatment guidelines for the management of hyperglycaemia.
5). There have been post-marketing cases of ketoacidosis with Signifor in patients with and without a history of diabetes. Patients who present with signs and symptoms consistent with severe metabolic acidosis should be assessed for ketoacidosis regardless of diabetes history.
In patients with poor glycaemic control (as defined by HbA1c values >8% while receiving anti-diabetic therapy), diabetes management and monitoring should be intensified prior to initiation and during pasireotide therapy. Liver tests Mild transient elevations in aminotransferases are commonly observed in patients treated with pasireotide.
8). Monitoring of liver function is recommended prior to treatment with pasireotide and after one, two, four, eight and twelve weeks during treatment. Thereafter liver function should be monitored as clinically indicated. Patients who develop increased transaminase levels should be monitored with a second liver function evaluation to confirm the finding.
If the finding is confirmed, the patient should be followed with frequent liver function monitoring until values return to pre-treatment levels. Therapy with pasireotide should be discontinued if the patient develops jaundice or other signs suggestive of clinically significant liver dysfunction, in the event of a sustained increase in AST (aspartate aminotransferase) or ALT of 5 x ULN or greater, or if ALT or AST elevations greater than 3 x ULN occur concurrently with bilirubin elevations greater than 2 x ULN.
This is not medical advice. Consult a qualified healthcare professional.
Who should not take it
GBOfficial regulatory label· Contraindications· revised May 1, 2026[1]
1. Severe hepatic impairment (Child Pugh C).
This is not medical advice. Consult a qualified healthcare professional.
1 Clinical Trials by Indication, Acromegaly). 2. 1 Clinical Trials by Indication, Cushing's disease). No patient administered SIGNIFOR LAR had a QTcF value of >500 ms in any of the pivotal clinical studies. 5. Post-Market Adverse Reactions The following adverse drug reactions have been derived from post-marketing experience with SIGNIFOR LAR.
Because these reactions were reported voluntarily from a population of uncertain size, it is not possible to reliably estimate their frequency Metabolism and nutrition disorders: Diabetic ketoacidosis.
Hepatobiliary Disorders:
Cholangitis Gastrointestinal Disorders: Malabsorption of dietary fat, Steatorrhea, Feces discolored including Feces pale 9. 2. Drug Interactions Overview Caution is required when co-administering SIGNIFOR LAR with drugs that are known to have hepatotoxic potential, or with anti-arrhythmic medicines and other drugs that may prolong the QT interval (see 7.
Warnings and Precautions). Medications that may disrupt electrolyte levels should be avoided when using SIGNIFOR LAR. SIGNIFOR LAR (Pasireotide for injectable suspension) Page 40 of 70 In vitro assessment of drug interactions: Pasireotide appears to be a substrate of efflux transporter P-gp (P-glycoprotein), but is not an inducer of P-gp.
In addition, at therapeutic dose levels, pasireotide is not expected to be: • A substrate of the efflux transporter BCRP (breast cancer resistance protein) nor of the influx transporters OCT1 (organic cation transporter 1) and OATP (organic anion- transporting polypeptide) 1B1, 1B3 or 2B1; • An inhibitor of UGT1A1 (uridine diphosphate glucuronosyltransferase 1A1), influx transporter OAT1 or OAT3, OATP 1B1 or 1B3, and OCT1 or OCT2, efflux transporter P- gp, BCRP, MRP2 (multi-drug resistance protein 2) or BSEP (bile salt export pump).
3. Drug-Behavioural Interactions Patients should be warned to exercise caution when driving or using machinery if they experience fatigue, headache, or dizziness during treatment with SIGNIFOR LAR. g. cigarette smoking, cannabis use, and/or alcohol consumption) has not been studied.
4. Drug-Drug Interactions No clinical drug-drug interaction studies have been performed with SIGNIFOR LAR.
General:
The lists below of potentially interacting drugs are not comprehensive. Current information sources should be consulted for newly approved drugs that prolong the QTc interval, decrease heart rate, prolong the PR interval, or cause electrolyte disturbances, as well as for older drugs for which these effects have recently been established.
Effect of Other Drugs on SIGNIFOR LAR QTc-Prolonging Drugs:
The concomitant use of SIGNIFOR LAR with another QTc-prolonging drug should be avoided (see 7. Warnings and Precautions – Cardiovascular and Monitoring and Laboratory Tests; 8. 2 Pharmacodynamics – Cardiac Electrophysiology). Drugs that have been associated with QTc interval prolongation and/or torsades de pointes include, but are not limited to, the examples in the following list.
Chemical/ pharmacological classes are listed if some, although not necessarily all, class members have been implicated in QTc prolongation and/or torsades de pointes: • Class IA, III, and 1C antiarrhythmics • antipsychotics • antidepressants • opioids • macrolide antibiotics and analogues • quinolone antibiotics • antimalarials • azole antifungals • dopamine receptor antagonists SIGNIFOR LAR (Pasireotide for injectable suspension) Page 41 of 70 • serotonin 5-hydroxytryptamine (5-HT3) receptor antagonists • tyrosine kinase inhibitors • histone deacetylase inhibitors • beta-2 adrenoceptor agonists Drugs that Decrease Heart Rate […]
This is not medical advice. Consult a qualified healthcare professional.
6 mg pasireotide by subcutaneous injection twice a day. Two months after the start of Signifor therapy, patients should be evaluated for clinical benefit. Patients who experience a significant reduction in urinary free cortisol (UFC) levels should continue to receive Signifor for as long as benefit is derived.
6 mg dose is well tolerated by the patient. Patients who have not responded to Signifor after two months of treatment should be considered for discontinuation. Management of suspected adverse reactions at any time during the treatment may require temporary dose reduction of Signifor.
3 mg twice a day is suggested. If a dose of Signifor is missed, the next injection should be administered at the scheduled time. Doses should not be doubled to make up for a missed dose. Switch from intramuscular to subcutaneous formulation There are no clinical data available on switching from the intramuscular to the subcutaneous 3 pasireotide formulation.
6 mg pasireotide twice a day. The patient should be monitored for response and tolerability and further dose adjustments may be needed. Special populations Paediatric population The safety and efficacy of Signifor in children and adolescents aged 0 to 18 years have not been established.
No data are available. 2). 2). Hepatic impairment Dose adjustment is not required in patients with mildly impaired hepatic function (Child Pugh A). 2). 6 mg twice a day. 4). Method of administration Signifor is to be administered subcutaneously by self injection.
Patients should receive instructions from the physician or a healthcare professional on how to inject Signifor subcutaneously. Use of the same injection site for two consecutive injections is not recommended. Sites showing signs of inflammation or irritation should be avoided.
Preferred injection sites for subcutaneous injections are the top of the thighs and the abdomen (excluding the navel or waistline). 6.
This is not medical advice. Consult a qualified healthcare professional.
Side effects & warnings
EUOfficial regulatory label· Adverse reactions· revised December 18, 2024[3]
Summary of the safety profile A total of 201 Cushing’s disease patients received Signifor in phase II and III studies. The safety profile of Signifor was consistent with the somatostatin analogue class, except for the occurrence of hypocortisolism and degree of hyperglycaemia.
The data described below reflect exposure of 162 Cushing’s disease patients to Signifor in the phase III study. 9 mg Signifor. 8%) were female. 3%) patients had persistent or recurrent Cushing’s disease and few (≤5%) in either treatment group had received previous pituitary irradiation.
0% of patients having at least six months’ exposure. 4% of patients. 5% of patients. Grade 3 and 4 adverse reactions were mostly related to hyperglycaemia. The most common adverse reactions (incidence ≥10%) were diarrhoea, nausea, abdominal pain, cholelithiasis, injection site reactions, hyperglycaemia, diabetes mellitus, fatigue and glycosylated haemoglobin increased.
Tabulated list of adverse reactions Adverse reactions reported up to the cut-off date of the analysis are presented in Table 1. Adverse reactions are listed according to MedDRA primary system organ class. Within each system organ class, adverse reactions are ranked by frequency.
Within each frequency grouping, adverse reactions are presented in the order of decreasing seriousness.
Frequencies were defined as follows:
Very common (≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); not known (cannot be estimated from the available data). 2% of patients) in the phase III study in Cushing’s disease patients. e. e. e. 30% at month 6). Mean fasting plasma glucose levels commonly increased within the first month of treatment, with decreases and stabilisation observed in subsequent months.
Fasting plasma glucose and HbA1c values generally decreased over the 28 days following pasireotide discontinuation but remained above baseline values. Long-term follow-up data are not available. Patients with baseline HbA1c ≥7% or who were taking antidiabetic medicinal products prior to randomisation tended to have higher mean changes in fasting plasma glucose and HbA1c relative to other patients.
5%) patients, respectively. One case of ketosis and one case of ketoacidosis have been reported during compassionate use of Signifor. 4). Gastrointestinal disorders Gastrointestinal disorders were frequently reported with Signifor. These reactions were usually of low grade, required no intervention and improved with continued treatment.
6% of patients enrolled in the phase III study in Cushing’s disease. Injection site reactions were also reported in clinical studies in other populations. The reactions were most frequently reported as local pain, erythema, haematoma, haemorrhage and pruritus.
These reactions resolved spontaneously and required no intervention. Liver enzymes Transient elevations in liver enzymes have been reported with the use of somatostatin analogues and were also observed in patients receiving pasireotide in clinical studies.
The elevations were mostly asymptomatic, of low grade and reversible with continued treatment. Rare cases of concurrent elevations in ALT greater than 3 x ULN and bilirubin greater than 2 x ULN have been observed. All cases of concurrent elevations were identified within ten days of initiation of treatment with Signifor.
The patients recovered without clinical sequelae and liver function test results […]
EUOfficial regulatory label· Warnings and precautions· revised December 18, 2024[3]
Glucose metabolism Alterations in blood glucose levels have been frequently reported in healthy volunteers and patients treated with pasireotide. 8). The degree of hyperglycaemia appeared to be higher in patients with pre-diabetic conditions or established diabetes mellitus.
8). 9 mg twice daily. e. glucagon-like peptide-1 [GLP-1] and glucose-dependent insulinotropic polypeptide [GIP]). Glycaemic status (fasting plasma glucose/haemoglobin A1c [FPG/HbA1c]) should be assessed prior to starting treatment with pasireotide.
FPG/HbA1c monitoring during treatment should follow established guidelines. Self monitoring of blood glucose and/or FPG assessments should be done weekly for the first two to three months and periodically thereafter, as clinically appropriate, as well as over the first two to four weeks after any dose increase.
In addition, monitoring of FPG 4 weeks and HbA1c 3 months after the end of the treatment should be performed. If hyperglycaemia develops in a patient being treated with Signifor, the initiation or adjustment of antidiabetic treatment is recommended, following the established treatment guidelines for the management of hyperglycaemia.
5). There have been post-marketing cases of ketoacidosis with Signifor in patients with and without a history of diabetes. Patients who present with signs and symptoms consistent with severe metabolic acidosis should be assessed for ketoacidosis regardless of diabetes history.
In patients with poor glycaemic control (as defined by HbA1c values >8% while receiving anti-diabetic therapy), diabetes management and monitoring should be intensified prior to initiation and during pasireotide therapy. Liver tests Mild transient elevations in aminotransferases are commonly observed in patients treated with pasireotide.
8). Monitoring of liver function is recommended prior to treatment with pasireotide and after one, two, four, eight and twelve weeks during treatment. Thereafter liver function should be monitored as clinically indicated. Patients who develop increased transaminase levels should be monitored with a second liver function evaluation to confirm the finding.
If the finding is confirmed, the patient should be followed with frequent liver function monitoring until values return to pre-treatment levels. Therapy with pasireotide should be discontinued if the patient develops jaundice or other signs suggestive of clinically significant liver dysfunction, in the event of a sustained increase in AST (aspartate aminotransferase) or ALT of 5 x ULN or greater, or if ALT or AST elevations greater than 3 x ULN occur concurrently with bilirubin elevations greater than 2 x ULN.
This is not medical advice. Consult a qualified healthcare professional.
Who should not take it
EUOfficial regulatory label· Contraindications· revised December 18, 2024[3]
1. Severe hepatic impairment (Child Pugh C).
This is not medical advice. Consult a qualified healthcare professional.
Following discontinuation of treatment with pasireotide, patients should be monitored until resolution. Treatment should not be restarted. 8). Careful monitoring is recommended in patients with cardiac disease and/or risk factors for bradycardia, such as history of clinically significant bradycardia or acute myocardial infarction, high-grade heart block, congestive heart failure (NYHA Class III or IV), unstable angina, sustained ventricular tachycardia, ventricular fibrillation.
5). Pasireotide has been shown to prolong the QT interval on the ECG in two dedicated healthy volunteer studies. The clinical significance of this prolongation is unknown. In clinical studies in Cushing’s disease patients, QTcF of >500 msec was observed in two out of 201 patients.
These episodes were sporadic and of single occurrence with no clinical consequence observed. Episodes of torsade de pointes were not observed either in those studies or in clinical studies in other patient populations. Pasireotide should be used with caution and the benefit risk carefully weighed in patients who are at significant risk of developing prolongation of QT, such as those: - with congenital long QT syndrome.
- with uncontrolled or significant cardiac disease, including recent myocardial infarction, congestive heart failure, unstable angina or clinically significant bradycardia. 5). - with hypokalaemia and/or hypomagnesaemia. Monitoring for an effect on the QTc interval is advisable and ECG should be performed prior to the start of Signifor therapy, one week after the beginning of the treatment and as clinically indicated thereafter.
Hypokalaemia and/or hypomagnesaemia must be corrected prior to administration of Signifor and should be monitored periodically during therapy. Hypocortisolism Treatment with Signifor leads to rapid suppression of ACTH (adrenocorticotropic hormone) secretion in Cushing’s disease patients.
Rapid, complete or near-complete suppression of ACTH may lead to a decrease in circulating […]
Following discontinuation of treatment with pasireotide, patients should be monitored until resolution. Treatment should not be restarted. 8). Careful monitoring is recommended in patients with cardiac disease and/or risk factors for bradycardia, such as history of clinically significant bradycardia or acute myocardial infarction, high-grade heart block, congestive heart failure (NYHA Class III or IV), unstable angina, sustained ventricular tachycardia, ventricular fibrillation.
5). Pasireotide has been shown to prolong the QT interval on the ECG in two dedicated healthy volunteer studies. The clinical significance of this prolongation is unknown. In clinical studies in Cushing’s disease patients, QTcF of >500 msec was observed in two out of 201 patients.
These episodes were sporadic and of single occurrence with no clinical consequence observed. Episodes of torsade de pointes were not observed either in those studies or in clinical studies in other patient populations. 5 Pasireotide should be used with caution and the benefit risk carefully weighed in patients who are at significant risk of developing prolongation of QT, such as those: - with congenital long QT syndrome.
- with uncontrolled or significant cardiac disease, including recent myocardial infarction, congestive heart failure, unstable angina or clinically significant bradycardia. 5). - with hypokalaemia and/or hypomagnesaemia. Monitoring for an effect on the QTc interval is advisable and ECG should be performed prior to the start of Signifor therapy, one week after the beginning of the treatment and as clinically indicated thereafter.
Hypokalaemia and/or hypomagnesaemia must be corrected prior to administration of Signifor and should be monitored periodically during therapy. Hypocortisolism Treatment with Signifor leads to rapid suppression of ACTH (adrenocorticotropic hormone) secretion in Cushing’s disease patients.
Rapid, complete or near-complete suppression of ACTH may lead to a decrease in […]