Medically reviewed by Drugs.com. Last updated on Jun 1, 2020.
(pas i REE oh tide)
- Pasireotide Diaspartate
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Subcutaneous, as diaspartate [strength expressed as base]:
Signifor: 0.3 mg/mL (1 mL); 0.6 mg/mL (1 mL); 0.9 mg/mL (1 mL)
Suspension Reconstituted ER, Intramuscular, as pamoate [strength expressed as base]:
Signifor LAR: 10 mg (1 ea); 30 mg (1 ea); 20 mg (1 ea); 40 mg (1 ea); 60 mg (1 ea)
Brand Names: U.S.
- Signifor LAR
- Somatostatin Analog
Pasireotide is a cyclohexapeptide somatostatin analog, which is a peptide inhibitor of multiple endocrine, neuroendocrine, and exocrine mechanisms. In patients with Cushing disease, pasireotide binds to somatostatin receptor (sst1-5), with high affinity for the sst1, sst2, sst3 subtypes, and highest affinity for the sst5 subtype, resulting in inhibition of ACTH secretion which leads to decreased cortisol secretion. In patients with acromegaly, pasireotide binds to sst2 and sst5, resulting in decreased GH and IGF-1.
Vd: >100 L
Primarily eliminated as unchanged drug hepatically (via biliary excretion)
Feces (~40% to 56%, primarily as unchanged drug); urine (~6% to 10%, primarily as unchanged drug)
Time to Peak
Plasma: Subcutaneous: 0.25 to 0.5 hours
Subcutaneous: ~12 hours
Special Populations: Hepatic Function Impairment
AUCinf was increased by 12%, 56%, and 42% and Cmax was increased by 3%, 46%, and 33%, respectively, in mild, moderate, and severe hepatic impairment (Child-Pugh class A, B, and C).
Use: Labeled Indications
Acromegaly (Signifor LAR): Treatment of acromegaly in patients who have had an inadequate response to surgery and/or for whom surgery is not an option.
The Acromegaly Consensus Group suggests use of pasireotide as a second-line therapy option in patients who have persistent disease despite surgical resection (or in whom surgery is not appropriate), normal glucose tolerance, and minimal/no response to first-line therapy (ACG [Melmed 2018]).
Cushing disease (Signifor and Signifor LAR): Treatment of Cushing disease in patients for whom pituitary surgery is not an option or has not been curative
There are no contraindications listed in the manufacturer's labeling.
Canadian labeling: Hypersensitivity to pasireotide or any component of the formulation; moderate or severe hepatic impairment (Child-Pugh B or C); uncontrolled diabetes (HbA1c ≥8%) despite receiving anti-diabetic therapy; NYHA Class III to IV heart failure; cardiogenic shock; second- or third-degree atrioventricular (AV) block, sinoatrial block, sick sinus syndrome (unless patient has a functioning pacemaker); severe bradycardia; congenital long QT syndrome or baseline QTc interval ≥500 ms.
Acromegaly (Signifor LAR): IM: Initial: 40 mg once every 28 days; for patients who have not normalized GH and/or IGF-1 levels after 3 months, may increase to a maximum of 60 mg once every 28 days. If adverse reactions occur or IFG-1 level decreases to less than lower limit of normal, decrease dosage (temporarily or permanently) by 20 mg decrements.
Missed dose: If a dose is missed, dose may be given up to but no later than 14 days prior to the next dose.
Initial: 0.6 mg or 0.9 mg twice daily.
Titrate based on response and tolerability. If adverse reactions occur, temporarily decrease dose by 0.3 mg increments. Recommended maintenance dosage range: 0.3 to 0.9 mg twice daily. Note: Maximum urinary free cortisol reductions are usually observed by 2 months of treatment.
Signifor LAR: IM: Initial: 10 mg once every 28 days; for patients who have not normalized 24-hour urinary free cortisol after 4 months, may increase dose (maximum: 40 mg once every 28 days). If adverse reactions occur or if cortisol level decreases to less than lower limit of normal or is in the lower normal range in patients with symptoms suggestive of adrenal insufficiency, may interrupt therapy (temporarily or permanently) or decrease to a previously tolerated dose.
Missed dose: If a dose is missed, dose may be given up to but no later than 14 days prior to the next dose.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Refer to adult dosing.
Signifor LAR: Allow to stand at room temperature for at least 30 minutes before reconstitution (maximum: 24 hours at room temperature). Reconstitute vials with provided diluent. Shake the vial moderately in a horizontal direction for at least 30 seconds until suspension is uniform; repeat moderate shaking for an additional 30 seconds if the powder is not completely suspended. Administer immediately after reconstitution.
IM: Signifor LAR: Administer only by IM injection into the left or right gluteus immediately after reconstitution.
SubQ: Signifor: Administer only by subcutaneous injection into the top of the thigh or abdomen (excluding the navel and waistline). Do not inject into inflamed or irritated skin. Alternate the injection site.
Signifor: Store at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F). Protect from light.
Signifor LAR: Prior to reconstitution: Store at 2°C to 8°C (36°F to 46°F). Do not freeze. Allow to stand at room temperature for at least 30 minutes before reconstitution (maximum: 24 hours at room temperature); administer immediately after reconstitution. The unreconstituted kit may be re-refrigerated, if needed.
Androgens: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
Antidiabetic Agents: May enhance the hypoglycemic effect of Hypoglycemia-Associated Agents. Monitor therapy
Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Monitor therapy
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Monitor therapy
Bromocriptine: Somatostatin Analogs may increase the serum concentration of Bromocriptine. Somatostatin Analogs may also delay bromocriptine absorption and time to maximum plasma concentrations. Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Consider therapy modification
Codeine: Somatostatin Analogs may decrease the metabolism of Codeine. The formation of two major codeine metabolites (morphine and norcodeine) may be impaired by somatostatin analogs. Monitor therapy
Copper Cu 64 Dotatate: Somatostatin Analogs may diminish the diagnostic effect of Copper Cu 64 Dotatate. Management: Imaging with copper Cu 64 dotatate positron emission tomography (PET) should be performed just prior to dosing with somatostatin analogs. If on somatostatin analogs, stop long-acting agents 28 days before, and short-acting agents 2 days before, imaging. Consider therapy modification
CycloSPORINE (Systemic): Somatostatin Analogs may decrease the serum concentration of CycloSPORINE (Systemic). Monitor therapy
Fexinidazole [INT]: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole [INT]. Avoid combination
Gallium Ga 68 Dotatate: Somatostatin Analogs may diminish the diagnostic effect of Gallium Ga 68 Dotatate. Specifically, a false negative PET scan may occur if Gallium GA 68 Dotatate is used during treatment with somatostatin analogs. Management: Imaging with gallium Ga 68 dotatate positron emission tomography (PET) should be performed just prior to dosing with long-acting somatostatin analogs. Short-acting somatostatin analogs can be used up to 24 hours before imaging with gallium Ga 68 dotatate. Consider therapy modification
Gallium Ga 68 Dotatoc: Somatostatin Analogs may diminish the diagnostic effect of Gallium Ga 68 Dotatoc. Management: Imaging with gallium Ga 68 dotatoc positron emission tomography (PET) should be performed just prior to dosing with long-acting somatostatin analogs. Short-acting somatostatin analogs can be used up to 24 hours before imaging with gallium Ga 68 dotatoc. Consider therapy modification
Haloperidol: QT-prolonging Agents (Indeterminate Risk - Caution) may enhance the QTc-prolonging effect of Haloperidol. Monitor therapy
Herbs (Hypoglycemic Properties): May enhance the hypoglycemic effect of Hypoglycemia-Associated Agents. Monitor therapy
Hypoglycemia-Associated Agents: May enhance the hypoglycemic effect of other Hypoglycemia-Associated Agents. Monitor therapy
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Monitor therapy
Lutetium Lu 177 Dotatate: Somatostatin Analogs may diminish the therapeutic effect of Lutetium Lu 177 Dotatate. Specifically, the therapeutic effect of Lutetium Lu 177 Dotatate may be diminished if the timing of Somatostatin Analog administration is not carried out as recommended. Management: Discontinue long-acting somatostatin analogs at least 4 weeks and short-acting octreotide at least 24 hours prior to lutetium Lu 177 dotatate dose. Administer short and long-acting octreotide during treatment as recommended. See full interaction monograph Consider therapy modification
Macimorelin: Somatostatin Analogs may diminish the diagnostic effect of Macimorelin. Avoid combination
Maitake: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy
Monoamine Oxidase Inhibitors: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
Pegvisomant: Somatostatin Analogs may enhance the adverse/toxic effect of Pegvisomant. Specifically, this combination may increase the risk for significant elevations of liver enzymes. Monitor therapy
Pegvisomant: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
Prothionamide: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
QT-prolonging Agents (Highest Risk): QT-prolonging Agents (Indeterminate Risk - Caution) may enhance the QTc-prolonging effect of QT-prolonging Agents (Highest Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Monitor therapy
Quinolones: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Quinolones may diminish the therapeutic effect of Agents with Blood Glucose Lowering Effects. Specifically, if an agent is being used to treat diabetes, loss of blood sugar control may occur with quinolone use. Monitor therapy
Ruxolitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. Monitor therapy
Salicylates: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
Selective Serotonin Reuptake Inhibitors: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Monitor therapy
Sincalide: Drugs that Affect Gallbladder Function may diminish the therapeutic effect of Sincalide. Management: Consider discontinuing drugs that may affect gallbladder motility prior to the use of sincalide to stimulate gallbladder contraction. Consider therapy modification
Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Consider therapy modification
Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Cardiovascular: Hypertension (8% to 15%), peripheral edema (10% to 14%)
Dermatologic: Alopecia (2% to 18%)
Endocrine & metabolic: Diabetes mellitus (immediate release: 6% to 20%; long-acting release: 21% to 31%), hypercholesterolemia (6% to 11%), hyperglycemia (29% to 47%), hypoglycemia (3% to 15%), increased gamma-glutamyl transferase (9% to 12%)
Gastrointestinal: Abdominal distension (5% to 12%), abdominal pain (8% to 25%), cholelithiasis (10% to 33%), decreased appetite (9% to 11%), diarrhea (immediate release: 58% to 59%; long-acting release: 16% to 39%), increased serum amylase (immediate release: 2%; long-acting release: 1% to 20%), increased serum lipase (immediate release: 6% to 9%; long-acting release: 1% to 30%), nausea (immediate release: 46% to 58%; long-acting release: 3% to 21%), upper abdominal pain (6% to 12%)
Hematologic & oncologic: Elevated glycosylated hemoglobin (5% to 12%), prolonged partial thromboplastin time (immediate release: 47%), prolonged prothrombin time (immediate release: 2% to 33%; long-acting release: 1%)
Hepatic: Increased serum alanine aminotransferase (≤14%), increased serum aspartate aminotransferase (≤14%)
Infection: Influenza (6% to 11%)
Local: Injection site reactions (immediate release: 17% to 18%; long-acting release: 2% to 7%)
Nervous system: Anxiety (immediate release: 6% to 11%), fatigue (10% to 27%), headache (immediate release: 28% to 29%; long-acting release: 3% to 19%), insomnia (immediate release: 4% to 14%)
Neuromuscular & skeletal: Asthenia (immediate release: 6% to 16%), back pain (5% to 11%), increased creatine phosphokinase in blood specimen (long-acting release: 13%), myalgia (5% to 12%)
Respiratory: Nasopharyngitis (6% to 16%)
1% to 10%:
Cardiovascular: Atrioventricular block (long-acting release: 6%), hypotension (6% to 8%), prolonged QT interval on ECG (1% to 6%), sinus bradycardia (3% to 10%)
Dermatologic: Pruritus (immediate release: 7% to 9%), xeroderma (immediate release: 6%)
Endocrine & metabolic: Adrenocortical insufficiency (2% to 7%), decreased cortisol, hyperuricemia (long-acting release: 7%), hypokalemia (immediate release: 5% to 7%), hypothyroidism (immediate release: 4%), impaired glucose tolerance/prediabetes, weight loss (long-acting release: 5%)
Gastrointestinal: Cholecystitis (long-acting release: 1%), cholestasis (long-acting release: 4%), constipation (5% to 9%), flatulence (long-acting release: 5%), pancreatitis (long-acting release: ≤1%), vomiting (3% to 10%)
Hematologic & oncologic: Anemia (3% to 6%)
Nervous system: Dizziness (2% to 10%), vertigo (immediate release: 5% to 8%)
Neuromuscular & skeletal: Arthralgia (6% to 10%), limb pain (5% to 7%)
Respiratory: Cough (long-acting release: 5%), upper respiratory tract infection (long-acting release: 7%)
<1%: Endocrine & metabolic: Diabetic ketoacidosis
Frequency not defined: Hepatic: Increased serum bilirubin
Endocrine & metabolic: Ketoacidosis (includes patients without a history of diabetes)
Concerns related to adverse effects:
• Cardiac disorders: Bradycardia and QT prolongation have been observed with therapy. Use with caution in patients with preexisting cardiac disease, patients with risk factors for bradycardia (eg, high-grade heart block, history of significant bradycardia, receiving concomitant drugs known to cause bradycardia), and/or patients at risk for QT prolongation (eg, congenital long QT, recent MI, heart failure, unstable angina, hypokalemia, hypomagnesemia, receiving concomitant drugs known to cause QT prolongation). Obtain baseline ECG prior to therapy and consider continued monitoring during therapy for an effect on the QTc interval. Correct hypokalemia, hypomagnesemia, and/or hypocalcemia prior to therapy and monitor during therapy.
• Cholelithiasis: Cholelithiasis and complications of cholelithiasis (eg, cholecystitis, cholangitis, pancreatitis) requiring cholecystectomy have been reported; monitor periodically for cholelithiasis; discontinue and treat appropriately if suspected.
• Hepatic effects: Increased liver enzymes have been reported; ALT, AST, and bilirubin should be monitored per recommendations in manufacturer's labeling. May require dosage interruption to investigate probable cause of confirmed or rising liver enzyme values; patients with significant elevations in liver function tests require more frequent monitoring and extensive monitoring (ALT, AST, alkaline phosphatase, total bilirubin).
• Hyperglycemia/diabetes/ketoacidosis: Inhibition of insulin and glucagon secretion may affect glucose regulation, leading to hyperglycemia (sometimes severe). Cases of ketoacidosis have been reported in patients with or without a history of diabetes; patients with predisposing factors, including acute illness, infection, pancreatic disorders (eg, pancreatic malignancy, pancreatic surgery), and alcohol abuse may be at greater risk. Exacerbation of glycemia occurred in the majority of patients during the initial months of therapy, including patients with normal glucose levels at baseline; diabetes and prediabetes has also been observed. Patients with poor baseline glycemic control are at higher risk of developing severe hyperglycemia. Prior to initiation, assess fasting blood glucose (FBG) levels and/or HbA1c, and optimize antidiabetic therapy in diabetic patients with poor baseline glycemic control. Patients should also do self-monitoring of blood glucose and/or FBG for the first few months of therapy, after dose increases, and periodically during use. If hyperglycemia occurs, initiation or dosage adjustment of antidiabetic therapy is recommended; if uncontrolled hyperglycemia persists despite antidiabetic therapy, consider dosage reduction or discontinuation of pasireotide. Following discontinuation of pasireotide, continued monitoring of blood glucose may be required if hypoglycemia is a risk. Assess patients presenting with signs and symptoms consistent with severe metabolic acidosis for ketoacidosis; discontinue pasireotide and promptly treat patients if ketoacidosis is suspected.
• Hypocortisolism: Suppression of the adrenocorticotropic hormone from therapy may lead to hypocortisolism in Cushing disease. Monitor all patients for signs or symptoms of hypocortisolism (eg, anorexia, fatigue, hypoglycemia, hyponatremia, hypotension, nausea, vomiting, weakness). If symptoms occur, consider stopping or reducing the dose until symptoms improve. Glucocorticoid replacement therapy may also be needed temporarily.
• Hypothyroidism: Decreases (slight) in thyroid function have been observed during therapy; monitor thyroid function tests prior to therapy and periodically during therapy.
• Pituitary hormone deficiency (anterior): May cause inhibition of anterior pituitary hormones; monitoring for pituitary deficiency is advised (eg, thyroid, adrenal, gonadal) prior to initiation of therapy and periodically thereafter. Patients who have undergone transsphenoidal surgery and pituitary irradiation are at an increased risk for deficiency.
• Diabetes: Prior to initiation, patients with poorly controlled or uncontrolled diabetes should have antidiabetic therapy optimized; exacerbation of glycemia commonly occurs with pasireotide use.
• Hepatic impairment: Use with caution in patients with hepatic impairment; lower doses are recommended at therapy initiation in patients with moderate impairment (Child-Pugh class B). Use not recommended in patients with severe impairment (Child-Pugh class C).
Acromegaly (Signifor LAR): Serum growth hormone (GH) and insulin-like growth factor (IGF-1) at 3 months prior to dosage adjustment and as clinically indicated; ECG (baseline; 21 days after injection in patients at high risk; consider continued monitoring during treatment); serum potassium and magnesium (prior to and periodically during therapy); thyroid function (baseline then periodically); adrenal function (prior to and periodically during therapy); gonadal function (prior to and periodically during therapy); signs and symptoms of adrenal insufficiency; heart rate (patients with cardiac disease and/or risk factor for bradycardia); monitor periodically for cholelithiasis.
Blood glucose and HbA1c: Prior to initiation, obtain fasting blood glucose and HbA1c; monitor blood glucose weekly for the first 3 months and every 4 to 6 weeks following dose increases, then periodically thereafter as appropriate. If glucose tolerance is consistently normal after 3 months of monitoring, may consider reduced monitoring (eg, HbA1c every 3 to 6 months [Coopmans 2019]). Following discontinuation of pasireotide, continued monitoring of blood glucose may be required if hypoglycemia is a risk.
Liver function tests: Prior to initiation, after the first 2 to 3 weeks, then monthly for 3 months and as clinically indicated; during therapy, discontinue if clinically significant liver impairment develops and monitor liver function until resolution.
Cushing disease: Urinary free cortisol (24-hour); FBG and HbA1c (prior to initiation); FBG and/or self-monitoring glucose (weekly for first 2 to 3 months, as well as over the first 2 to 4 weeks after any dose increase, then periodically during therapy), and FBG or HbA1c (following discontinuation as clinically appropriate); serum GH and IGF-1 (baseline then periodically); thyroid function (baseline then periodically); potassium and magnesium (prior to therapy then periodically during therapy); ECG (baseline and consider continued monitoring during treatment); gall bladder ultrasonography (baseline, then every 6 to 12 months during therapy); signs and symptoms of hypocortisolism (eg, weakness, fatigue, nausea, vomiting); heart rate.
Liver function tests:
Signifor: Prior to therapy, 1 to 2 weeks after initiation, then monthly for 3 months, then every 6 months thereafter; more frequent testing may be necessary:
If ALT normal at baseline and ALT increases 3 to 5 times ULN on therapy: Repeat ALT within 1 week
If ALT normal at baseline and ALT increases >5 times ULN on therapy: Repeat ALT within 48 hours
If ALT abnormal at baseline and ALT increases 3 to 5 times baseline values on therapy: Repeat ALT within 1 week
If ALT abnormal at baseline and ALT increases >5 times ULN on therapy: Repeat ALT <1 week
Note: ALT levels should be done in a laboratory capable of same-day results; if ALT levels are confirmed or rising, interrupt therapy and investigate cause.
During therapy, if any liver test ≥5 times ULN (with a normal baseline) OR >5 times the baseline value (with an abnormal baseline), interrupt therapy and monitor ALT, AST, alkaline phosphatase, and total bilirubin weekly or more frequently. If values return to normal or near normal, therapy may be reinitiated with extreme caution/monitoring only if another likely cause for hepatic effects discovered.
Signifor LAR: Prior to initiation, after the first 2 to 3 weeks, then monthly for 3 months and as clinically indicated; during therapy, discontinue if clinically significant liver impairment develops and monitor liver function until resolution.
Fertility may be improved with treatment in females of reproductive potential following normalization of serum cortisol in patients with Cushing disease, and normalization of insulin-like growth factor 1 and growth hormone in women with acromegaly. The Endocrine Society acromegaly guidelines recommend women of childbearing potential use adequate contraception during treatment, and suggest discontinuing long-acting formulations of somatostatin analogs approximately 2 months prior to a planned pregnancy; short-acting octreotide may be used until conception if needed (Endocrine Society [Katznelson 2014]).
If treatment for acromegaly is required during pregnancy for worsening symptoms (eg, headaches or evidence of worsening tumor), alternative agents are recommended. Monitoring of insulin-like growth factor 1 (IGF-1) and/or growth hormone (GH) is not recommended during pregnancy, as an active placental GH variant present in maternal blood limits the usefulness of the results (Endocrine Society [Katznelson 2014]).
What is this drug used for?
• It is used to treat Cushing disease.
• It is used to treat acromegaly.
All drugs may cause side effects. However, many people have no side effects or only have minor side effects. Call your doctor or get medical help if any of these side effects or any other side effects bother you or do not go away:
• Constipation, diarrhea, stomach pain, upset stomach, throwing up, or feeling less hungry
• Feeling tired or weak
• Signs of a common cold
• Pain in arms or legs
• Hair loss
• Nose or throat irritation
• Irritation where the shot is given
• Flu-like signs
• Back, muscle, or joint pain
• Trouble sleeping
• Dry skin
WARNING/CAUTION: Even though it may be rare, some people may have very bad and sometimes deadly side effects when taking a drug. Tell your doctor or get medical help right away if you have any of the following signs or symptoms that may be related to a very bad side effect:
• Liver problems like dark urine, feeling tired, not hungry, upset stomach or stomach pain, light-colored stools, throwing up, or yellow skin or eyes
• Electrolyte problems like mood changes, confusion, muscle pain or weakness, a heartbeat that does not feel normal, seizures, not hungry, or very bad upset stomach or throwing up
• High or low blood sugar like breath that smells like fruit, dizziness, fast breathing, fast heartbeat, feeling confused, feeling sleepy, feeling weak, flushing, headache, more thirsty or hungry, passing urine more often, shaking, or sweating
• Gallbladder problems like pain in the upper right belly area, right shoulder area, or between the shoulder blades; yellow skin or eyes; fever with chills; bloating; or very upset stomach or throwing up
• High or low blood pressure like very bad headache or dizziness, passing out, or change in eyesight
• Decreased hormones like abnormal diarrhea, weight loss, passing out, severe or lasting dizziness, tiredness, weakness, nausea, upset stomach, throwing up, or loss of appetite
• Fast heartbeat, a heartbeat that does not feel normal, or pass out
• Slow heartbeat
• Swelling in the arms or legs
• Swelling of belly
• Signs of an allergic reaction, like rash; hives; itching; red, swollen, blistered, or peeling skin with or without fever; wheezing; tightness in the chest or throat; trouble breathing, swallowing, or talking; unusual hoarseness; or swelling of the mouth, face, lips, tongue, or throat.
Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.
Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a limited summary of general information about the medicine's uses from the patient education leaflet and is not intended to be comprehensive. This limited summary does NOT include all information available about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not intended to provide medical advice, diagnosis or treatment and does not replace information you receive from the healthcare provider. For a more detailed summary of information about the risks and benefits of using this medicine, please speak with your healthcare provider and review the entire patient education leaflet.
Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.
More about pasireotide
- Side Effects
- During Pregnancy or Breastfeeding
- Dosage Information
- Drug Interactions
- En Español
- Drug class: somatostatin and somatostatin analogs