H.P. Acthar

ACTH and Analogs

The repository corticotropin (ACTH) gel injection is not for intravenous use; administer by intramuscular or subcutaneous routes only.
Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.

Allow the repository gel injection to reach room temperature before administration. Caution should be taken not to over-pressurize the vial prior to withdrawing the product.
Inject deeply into a large muscle mass. Rotate sites of injection.

Allow the repository gel injection to reach room temperature before administration. Caution should be taken not to over-pressurize the vial prior to withdrawing the product.
Inject subcutaneously, taking care not to inject intradermally. Rotate injection sites.

seizures / Delayed / 3.0-12.0
skin atrophy / Delayed / Incidence not known
esophageal ulceration / Delayed / Incidence not known
GI perforation / Delayed / Incidence not known
GI bleeding / Delayed / Incidence not known
pancreatitis / Delayed / Incidence not known
scarlatiniform exanthema / Rapid / Incidence not known
anaphylactic shock / Rapid / Incidence not known
ocular hypertension / Delayed / Incidence not known
heart failure / Delayed / Incidence not known
atrial fibrillation / Early / Incidence not known
vasculitis / Delayed / Incidence not known
papilledema / Delayed / Incidence not known
intracranial bleeding / Delayed / Incidence not known
avascular necrosis / Delayed / Incidence not known
bone fractures / Delayed / Incidence not known

Cushing's syndrome / Delayed / 3.0-22.0
hypertension / Early / 11.0-19.0
constipation / Delayed / 0-5.0
candidiasis / Delayed / 2.0
erythema / Early / Incidence not known
impaired wound healing / Delayed / Incidence not known
esophagitis / Delayed / Incidence not known
hypotension / Rapid / Incidence not known
wheezing / Rapid / Incidence not known
exophthalmos / Delayed / Incidence not known
ocular infection / Delayed / Incidence not known
cataracts / Delayed / Incidence not known
sodium retention / Delayed / Incidence not known
peripheral edema / Delayed / Incidence not known
hypokalemia / Delayed / Incidence not known
edema / Delayed / Incidence not known
metabolic alkalosis / Delayed / Incidence not known
fluid retention / Delayed / Incidence not known
palpitations / Early / Incidence not known
euphoria / Early / Incidence not known
depression / Delayed / Incidence not known
psychosis / Early / Incidence not known
subdural hematoma / Early / Incidence not known
pseudotumor cerebri / Delayed / Incidence not known
EEG changes / Delayed / Incidence not known
hyperglycemia / Delayed / Incidence not known
hypothalamic-pituitary-adrenal (HPA) suppression / Delayed / Incidence not known
withdrawal / Early / Incidence not known
osteoporosis / Delayed / Incidence not known
osteopenia / Delayed / Incidence not known
myasthenia / Delayed / Incidence not known
growth inhibition / Delayed / Incidence not known

infection / Delayed / 20.0-46.0
irritability / Delayed / 7.0-19.0
acne vulgaris / Delayed / 14.0-14.0
diarrhea / Early / 3.0-14.0
rash / Early / 8.0-8.0
fever / Early / 5.0-8.0
vomiting / Early / 3.0-5.0
nasal congestion / Early / 1.0-5.0
injection site reaction / Rapid / Incidence not known
ecchymosis / Delayed / Incidence not known
hyperhidrosis / Delayed / Incidence not known
petechiae / Delayed / Incidence not known
nausea / Early / Incidence not known
urticaria / Rapid / Incidence not known
pruritus / Rapid / Incidence not known
dizziness / Early / Incidence not known
emotional lability / Early / Incidence not known
fatigue / Early / Incidence not known
insomnia / Early / Incidence not known
malaise / Early / Incidence not known
lethargy / Early / Incidence not known
asthenia / Delayed / Incidence not known
headache / Early / Incidence not known
vertigo / Early / Incidence not known
menstrual irregularity / Delayed / Incidence not known
hirsutism / Delayed / Incidence not known

Acthar, CORTROPHIN

Rx

Parenteral adrenocorticotropic hormone (ACTH); highly purified and extracted from porcine pituitary glands
Repository injection primarily used in adults for multiple sclerosis; other corticosteroids usually preferred for other indications
In pediatric patients, repository injection primarily used for infantile spasms in infants and children less than 2 years

75 units/m2/dose intramuscularly twice daily for 2 weeks is the FDA-approved regimen. The dose should then be tapered over a 2 week period to avoid adrenal insufficiency. The FDA-approved product label suggests the following tapering schedule: 30 units/m2/dose intramuscularly every morning for 3 days, 15 units/m2/dose intramuscularly every morning for 3 days, 10 units/m2/dose intramuscularly every morning for 3 days, and 10 units/m2/dose intramuscularly every other morning for 6 days. Body surface area should be calculated with the following formula: BSA (m2) = the square root of ([height (cm) x weight (kg)]/3,600). Various other non-FDA-approved regimens have been used off label. Low doses of 5 to 40 units/day intramuscularly for 1 to 6 weeks have been recommended by some neurologists, whereas others recommend larger doses of 40 to 160 units/day intramuscularly for 3 to 12 months. In 1 study, no major difference in efficacy was found between low doses for short periods and large doses for longer periods of time; however, hypertension was more common with the larger doses. In this study, the low-dose regimen was 20 units/day intramuscularly for 2 weeks. If the patient responded, the dose was tapered and discontinued over a 1-week period. If the patient did not respond, the dose was increased to 30 units/day intramuscularly for 4 weeks, then tapered and discontinued over a 1-week period. The high-dose regimen was 150 units/m2/day intramuscularly for 3 weeks; the dose was then tapered and discontinued over 9 weeks.

80 to 120 units/day IM or subcutaneously for 2 to 3 weeks. It may be necessary to taper the dose.

40 to 80 units subcutaneously or IM every 24 to 72 hours. Individualize the dose and dosing frequency after considering the disease severity, patient response, and plasma and urine corticosteroid concentrations. After prolonged use, a gradual taper may be necessary in order to avoid adrenal insufficiency or recurrent symptoms. Selected cases may require low-dose maintenance therapy.

40 to 80 units IM or subcutaneously every 24 to 72 hours. Individualize the dose and dosing frequency after considering the disease severity, patient response, and plasma and urine corticosteroid concentrations. After prolonged use, a gradual taper may be necessary in order to avoid adrenal insufficiency or recurrent symptoms.

40 to 80 units IM or subcutaneously every 24 to 72 hours. Individualize the dose and dosing frequency after considering the disease severity, patient response, and plasma and urine corticosteroid concentrations. After prolonged use, a gradual taper may be necessary in order to avoid adrenal insufficiency or recurrent symptoms.

40 to 80 units IM or subcutaneously every 24 to 72 hours. Individualize the dose and dosing frequency after considering the disease severity, patient response, and plasma and urine corticosteroid concentrations. After prolonged use, a gradual taper may be necessary in order to avoid adrenal insufficiency or recurrent symptoms.

40 to 80 units IM or subcutaneously every 24 to 72 hours. Individualize the dose and dosing frequency after considering the disease severity, patient response, and plasma and urine corticosteroid concentrations. After prolonged use, a gradual taper may be necessary in order to avoid adrenal insufficiency or recurrent symptoms.

The usual dose is 40 to 80 units given subcutaneously or IM every 24 to 72 hours. Individualize the dose and dosing frequency after considering the disease severity, patient response, and plasma and urine corticosteroid concentrations. After prolonged use, a gradual taper may be necessary in order to avoid adrenal insufficiency or recurrent symptoms. Selected cases may require low-dose maintenance therapy. Guidelines support use for symptomatic relief and acute symptoms.

Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.

Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

Aliskiren; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Amiloride: (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Amiloride; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss. (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Amlodipine; Valsartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Atenolol; Chlorthalidone: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Azilsartan; Chlorthalidone: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Benazepril; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Bisoprolol; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Bumetanide: (Minor) Monitor potassium concentrations during concomitant corticotropin and loop diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and loop diuretics cause increased renal potassium loss.
Calcium Carbonate: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. Patients taking systemic corticosteroids should ensure proper intake of calcium as directed by their health care provider.
Calcium Carbonate; Famotidine; Magnesium Hydroxide: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. Patients taking systemic corticosteroids should ensure proper intake of calcium as directed by their health care provider.
Calcium Carbonate; Magnesium Hydroxide: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. Patients taking systemic corticosteroids should ensure proper intake of calcium as directed by their health care provider.
Calcium Carbonate; Magnesium Hydroxide; Simethicone: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. Patients taking systemic corticosteroids should ensure proper intake of calcium as directed by their health care provider.
Calcium Carbonate; Simethicone: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. Patients taking systemic corticosteroids should ensure proper intake of calcium as directed by their health care provider.
Calcium; Vitamin D: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. Patients taking systemic corticosteroids should ensure proper intake of calcium as directed by their health care provider.
Candesartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Captopril; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Chlorothiazide: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Chlorthalidone: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Chlorthalidone; Clonidine: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Daratumumab; Hyaluronidase: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Efgartigimod Alfa; Hyaluronidase: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Enalapril; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Eprosartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Ethacrynic Acid: (Minor) Monitor potassium concentrations during concomitant corticotropin and loop diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and loop diuretics cause increased renal potassium loss.
Fosinopril; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Furosemide: (Minor) Monitor potassium concentrations during concomitant corticotropin and loop diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and loop diuretics cause increased renal potassium loss.
Hyaluronidase, Recombinant; Immune Globulin: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Hyaluronidase: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Hydrochlorothiazide, HCTZ; Methyldopa: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Hydrochlorothiazide, HCTZ; Moexipril: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Indapamide: (Minor) Monitor potassium concentrations during concomitant corticotropin and indapamide use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and indapamide cause increased renal potassium loss.
Irbesartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Lisinopril; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Loop diuretics: (Minor) Monitor potassium concentrations during concomitant corticotropin and loop diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and loop diuretics cause increased renal potassium loss.
Losartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Methyclothiazide: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Metolazone: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Metoprolol; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Olmesartan; Amlodipine; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Olmesartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Pertuzumab; Trastuzumab; Hyaluronidase: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Potassium-sparing diuretics: (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Propranolol; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Quinapril; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Rituximab; Hyaluronidase: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Spironolactone: (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Spironolactone; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss. (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Telmisartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Thiazide diuretics: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.
Torsemide: (Minor) Monitor potassium concentrations during concomitant corticotropin and loop diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and loop diuretics cause increased renal potassium loss.
Trastuzumab; Hyaluronidase: (Minor) Corticosteroids (e.g., cortisone, corticotropin, ACTH), when given in large systemic doses, may render tissues partially resistant to the action of hyaluronidase. Patients receiving these medications may require larger amounts of hyaluronidase for equivalent dispersing effect.
Triamterene: (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Triamterene; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss. (Minor) Monitor serum electrolytes, particularly serum calcium concentrations, during concomitant corticotropin and potassium-sparing diuretic use. Corticotropin may accentuate the electrolyte loss associated with diuretic therapy.
Valsartan; Hydrochlorothiazide, HCTZ: (Minor) Monitor potassium concentrations during concomitant corticotropin and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticotropin and thiazide diuretics cause increased renal potassium loss.

Acthar/Corticotropin (Porcine)/CORTROPHIN Intramuscular Inj Sol: 1mL, 80U
Acthar/Corticotropin (Porcine)/CORTROPHIN Subcutaneous Inj Sol: 1mL, 80U

80 units/day subcutaneous or IM for most conditions; up to 120 units/day IM for multiple sclerosis exacerbations.

80 units/day subcutaneous or IM for most conditions; up to 120 units/day IM for multiple sclerosis exacerbations.

80 units/day subcutaneous or IM.

2 years and older: 80 units/day subcutaneously or IM.
Less than 2 years: 150 units/m2/day IM.

150 units/m2/day IM.

Safety and efficacy have not been established.

Corticotropin and endogenous ACTH stimulates steroidogenesis and the release of cortisol (hydrocortisone), corticosterone, and weak androgens from the adrenal cortex. The physiologic and pharmacologic effects of corticotropin are due primarily to the glucocorticoid cortisol, which also has some mineralocorticoid activity. Prolonged administration of large doses of corticotropin induces hyperplasia and hypertrophy of the adrenal cortex and continuous high output of cortisol, corticosterone and weak androgens. The release of endogenous ACTH is under the influence of the nervous system via the regulatory hormone released from the hypothalamus and by a negative corticosteroid feedback mechanism. Elevated plasma cortisol suppresses ACTH release. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, collectively called lipocortins; lipocortins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor molecule arachidonic acid. Other effects of corticotropin include extra-adrenal effects such as binding to melanocortin receptors.
 
Although oral glucocorticoids do not depend on adrenal function for effectiveness, have a more predictable profile, and have easily regulated doses for patient-specific therapy, corticotropin therapy is preferred by some clinicians in certain conditions.
 
The mechanism of action of corticotropin for the treatment of infantile spasms is unknown.

Corticotropin (ACTH) is administered subcutaneously and intramuscularly. Corticotropin is available as a repository corticotropin injection (RCI). ACTH rapidly disappears from the circulation following its intravenous administration; in humans, the plasma half-life is about 15 minutes. The pharmacokinetics of the repository corticotropin injection have not been adequately characterized. The maximal effects of a trophic hormone on a target organ are achieved when optimal amounts of hormone are acting continuously. Thus, a fixed dose of the repository corticotropin injection will demonstrate a linear increase in adrenocortical secretion with increasing duration of an infusion.
 
Affected cytochrome P450 isoenzymes and drug transporters: None known

Corticotropin, ACTH may cause fetal harm when administered to a patient during pregnancy due to stimulation of an endogenous steroid response. Use of corticosteroids during pregnancy has been associated with intrauterine growth restriction, decreased birth weight and preterm birth; thus there is potential concern regarding use of corticotropin in pregnancy. Hypoadrenalism has also been reported in infants born to patients who received high-dose and/or long-term corticosteroid therapy during pregnancy. Corticotropin has not been adequately studied in animals to determine risk of therapy during pregnancy. Closely monitor infants exposed to corticotropin during pregnancy for signs of hypoadrenalism, such as poor feeding, irritability, weakness, and vomiting. Adrenocortical disease during pregnancy is relatively rare as most cases are diagnosed before a woman becomes pregnant, but ACTH stimulated normal cortisol values have been established for each trimester. Adrenal disease may cause significant maternal and fetal morbidity, so accurate and rapid diagnosis is important. The use of cosyntropin to confirm the diagnosis of adrenal insufficiency during pregnancy, when suspected, is described in the literature.

There are no available data on the presence of corticotropin, ACTH in human milk, the effects on the breastfed infant, or on milk production. Because many drugs are excreted in human milk and due to the potential for serious adverse reactions in nursing infants, the manufacturer states that a decision should be made whether to discontinue breast-feeding or to discontinue the drug, taking into account the importance of the drug to the mother and the indication for use. However, due to its large molecular weight and short half-life of only 10 to 15 minutes, corticotropin, ACTH is unlikely to appear in human milk. It is also unlikely that corticotropin, ACTH would be absorbed by the infant because it would probably be degraded in the infant's gastrointestinal tract. Animal data suggests an increase in breast milk cortisol levels might be expected after administration of corticotropin to a nursing mother. However, if corticotropin is required in the mother, it is not a reason to discontinue breast-feeding. Alternative therapies to consider include other corticosteroids, such as prednisone and methylprednisolone. Prednisone concentrations in breast milk are low, and no adverse effects have been reported in the breast-fed infant with maternal use of any corticosteroid during breast-feeding; prednisone is generally considered compatible to use during lactation.