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ATACAND HCT
Overview
What is ATACAND HCT?
ATACAND HCT (candesartan cilexetil-hydrochlorothiazide) combines an angiotensin II receptor (type AT) antagonist and a diuretic, hydrochlorothiazide.
Candesartan cilexetil, a nonpeptide, is chemically described as (±)-1-Hydroxyethyl 2-ethoxy-1-[-(-1-tetrazol-5-ylphenyl)benzyl]-7-benzimidazolecarboxylate, cyclohexyl carbonate (ester).
Its empirical formula is CHNO, and its structural formula is
Candesartan cilexetil is a white to off-white powder with a molecular weight of 610.67. It is practically insoluble in water and sparingly soluble in methanol. Candesartan cilexetil is a racemic mixture containing one chiral center at the cyclohexyloxycarbonyloxy ethyl ester group. Following oral administration, candesartan cilexetil undergoes hydrolysis at the ester link to form the active drug, candesartan, which is achiral.
Hydrochlorothiazide is 6-chloro-3,4-dihydro-2-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. Its empirical formula is CHClNOS and its structural formula is
Hydrochlorothiazide is a white, or practically white, crystalline powder with a molecular weight of 297.72, which is slightly soluble in water, but freely soluble in sodium hydroxide solution.
ATACAND HCT is available for oral administration in three tablet strengths of candesartan cilexetil and hydrochlorothiazide.
ATACAND HCT 16-12.5 contains 16 mg of candesartan cilexetil and 12.5 mg of hydrochlorothiazide. ATACAND HCT 32-12.5 contains 32 mg of candesartan cilexetil and 12.5 mg of hydrochlorothiazide. ATACAND HCT 32–25 contains 32 mg of candesartan cilexetil and 25 mg of hydrochlorothiazide. The inactive ingredients of the tablets are carboxymethylcellulose calcium, hydroxypropyl cellulose, lactose monohydrate, magnesium stearate, cornstarch, polyethylene glycol 8000, and ferric oxide (yellow). Ferric oxide (reddish brown) is also added to the 16-12.5 mg and 32–25 mg tablets as colorant.
What does ATACAND HCT look like?
What are the available doses of ATACAND HCT?
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What should I talk to my health care provider before I take ATACAND HCT?
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How should I use ATACAND HCT?
ATACAND HCT is indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including the class to which this drug principally belongs. There are no controlled trials demonstrating risk reduction with ATACAND HCT.
Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. Many patients will require more than one drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program’s Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC).
Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly.
Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal.
Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g., on angina, heart failure, or diabetic kidney disease). These considerations may guide selection of therapy.
This fixed dose combination is not indicated for initial therapy (see ).
The usual recommended starting dose of candesartan cilexetil is 16 mg once daily when it is used as monotherapy in patients who are not volume depleted. ATACAND can be administered once or twice daily with total daily doses ranging from 8 mg to 32 mg. Patients requiring further reduction in blood pressure should be titrated to 32 mg. Doses larger than 32 mg do not appear to have a greater blood pressure lowering effect.
Hydrochlorothiazide is effective in doses of 12.5 to 50 mg once daily.
Use in Renal Impairment: Dosing recommendations for ATACAND HCT in patients with creatinine clearance < 30 mg/min cannot be provided (see ).
Use in moderate to severe Hepatic Impairment: ATACAND HCT is not recommended for initiation because the appropriate starting dose, 8 mg, cannot be given (see ).
Replacement Therapy:
Dose Titration by Clinical Effect:
A patient whose blood pressure is not controlled on 32 mg of ATACAND can expect incremental blood pressure effects from ATACAND HCT 32-12.5 mg and then 32-25 mg. The maximal antihypertensive effect of any dose of ATACAND HCT can be expected within 4 weeks of initiating that dose.
ATACAND HCT may be administered with other antihypertensive agents.
ATACAND HCT may be administered with or without food.
What interacts with ATACAND HCT?
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What are the warnings of ATACAND HCT?
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What are the precautions of ATACAND HCT?
Metabolic Disturbances
Hydrochlorothiazide may alter glucose tolerance and raise serum levels of cholesterol and triglycerides.
Hydrochlorothiazide may raise the serum uric acid level due to reduced clearance of uric acid and may cause or exacerbate hyperuricemia and precipitate gout in susceptible patients.
Thiazides decrease urinary calcium excretion and may cause elevation of serum calcium. Avoid using ATACAND HCT in patients with hypercalcemia.
Systemic Lupus Erythematosus
Thiazide diuretics have been reported to cause exacerbation or activation of systemic lupus erythematosus.
Information for Patients
Drug Interactions
Because candesartan is not significantly metabolized by the cytochrome P450 system and at therapeutic concentrations has no effects on P450 enzymes, interactions with drugs that inhibit or are metabolized by those enzymes would not be expected.
Interactions common to both Candesartan Cilexetil and Hydrochlorothiazide
Non-Steroidal Anti-Inflammatory Agents including Selective Cyclooxygenase-2 Inhibitors (COX-2 Inhibitors)
The antihypertensive effect of angiotensin II receptor antagonists, including candesartan may be attenuated by NSAIDs including selective COX-2 inhibitors.
Lithium
Interactions with Candesartan Cilexetil
Dual Blockade of the Renin-Angiotensin System (RAS)
Dual blockade of the RAS with angiotensin receptor blockers, ACE inhibitors, or aliskiren is associated with increased risks of hypotension, hyperkalemia, and changes in renal function (including acute renal failure) compared to monotherapy. Closely monitor blood pressure, renal function and electrolytes in patients on ATACAND HCT and other agents that affect the RAS.
Co-administration of ATACAND HCT with potassium sparing diuretics, potassium supplements, potassium-containing salt substitutes or other drugs that raise serum potassium levels may result in hyperkalemia. Monitor serum potassium in such patients.
Do not co-administer aliskiren with ATACAND HCT in patients with diabetes. Avoid use of aliskiren with ATACAND HCT in patients with renal impairment (GFR <60 ml/min) (see ).
Interactions with Hydrochlorothiazide
Alcohol, barbiturates, or narcotics − Potentiation of orthostatic hypotension may occur.
Antidiabetic drugs (oral agents and insulin) − Dosage adjustment of the antidiabetic drug may be required.
Diazoxide − the hyperglycemic effect of diazoxide may be enhanced by thiazides.
Ion Exchange resins − Single doses of either cholestyramine or colestipol resins bind the hydrochlorothiazide and reduce its absorption from the gastrointestinal tract by up to 85% and 43%, respectively. Stagger the dosage of hydrochlorothiazide and ion exchange resins such that hydrochlorothiazide is administered at least 4 hours before or 4-6 hours after the administration of resins.
Skeletal muscle relaxants, nondepolarizing (e.g., tubocurarine) − Possible increased responsiveness to muscle relaxants such as curare derivatives.
Digitalis − Thiazide-induced hypokalemia or hypomagnesemia may predispose to digoxin toxicity.
Noradrenaline – Thiazides may decrease arterial responsiveness to noradrenaline, but not enough to preclude effectiveness of the pressor agent for therapeutic use.
Steroids or Adrenocorticotropic Hormone – Hypokalemia may develop during concomitant use of steroids or adrenocorticotropic hormone (ACTH).
Cytotoxic products – Thiazides may reduce the renal excretion of cytotoxic medicinal products (e.g. cyclophosphamide, methotrexate) and potentiate their myelosuppressive effects.
Cyclosporine − Concomitant treatment with cyclosporine may increase the risk of hyperuricemia and gout-type complications.
Carcinogenesis, Mutagenesis, Impairment of Fertility
No carcinogenicity studies have been conducted with the combination of candesartan cilexetil and hydrochlorothiazide. There was no evidence of carcinogenicity when candesartan cilexetil was orally administered to mice and rats for up to 104 weeks at doses up to 100 and 1000 mg/kg/day, respectively. Rats received the drug by gavage whereas mice received the drug by dietary administration. These (maximally-tolerated) doses of candesartan cilexetil provided systemic exposures to candesartan (AUCs) that were, in mice, approximately 7 times and, in rats, more than 70 times the exposure in man at the maximum recommended daily human dose (32 mg). Two-year feeding studies in mice and rats conducted under the auspices of the National Toxicology Program (NTP) uncovered no evidence of a carcinogenic potential of hydrochlorothiazide in female mice (at doses of up to approximately 600 mg/kg/day) or in male and female rats (at doses of up to approximately 100 mg/kg/day). The NTP, however, found equivocal evidence for hepatocarcinogenicity in male mice.
Candesartan cilexetil or candesartan (the active metabolite), in combination with hydrochlorothiazide, tested positive in the Chinese hamster lung (CHL) chromosomal aberration assay and mouse lymphoma mutagenicity assay. The candesartan cilexetil/hydrochlorothiazide combination tested negative for mutagenicity in bacteria (Ames test), for unscheduled DNA synthesis in rat liver, for chromosomal aberrations in rat bone marrow and for micronuclei in mouse bone marrow.
Both candesartan and its O-deethyl metabolite tested positive for genotoxicity in the CHL chromosomal aberration assay. Neither compound tested positive in the Ames microbial mutagenesis assay or in the mouse lymphoma cell assay. Candesartan (but not its O-deethyl metabolite) was also evaluated in the mouse micronucleus test and in the Chinese hamster ovary (CHO) gene mutation assay, in both cases with negative results. Candesartan cilexetil was evaluated in the Ames test, the mouse lymphoma cell assay, the rat hepatocyte unscheduled DNA synthesis assay and the mouse micronucleus test, in each case with negative results. Candesartan cilexetil was not evaluated in the CHL chromosomal aberration or CHO gene mutation assays.
When hydrochlorothiazide was tested alone, positive results were obtained in the CHO sister chromatid exchange (clastogenicity) and mouse lymphoma cell (mutagenicity) assays and in the non-disjunction assay. Hydrochlorothiazide was not genotoxic in the Ames test for point mutations and the CHO test for chromosomal aberrations, or in assays using mouse germinal cell chromosomes, Chinese hamster bone marrow chromosomes, and the Drosophila sex-linked recessive lethal trait gene.
No fertility studies have been conducted with the combination of candesartan cilexetil and hydrochlorothiazide. Fertility and reproductive performance were not affected in studies with male and female rats given oral doses of up to 300 mg candesartan cilexetil/kg/day (83 times the maximum daily human dose of 32 mg on a body surface area basis). Hydrochlorothiazide had no adverse effects on the fertility of mice and rats of either sex in studies wherein these species were exposed, via their diet, to doses of up to 100 and 4 mg/kg, respectively, prior to conception and throughout gestation.
Nursing Mothers
It is not known whether candesartan is excreted in human milk, but candesartan has been shown to be present in rat milk. Thiazides appear in human milk. Because of the potential for adverse effects on the nursing infant, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.
Pediatric Use
Neonates with a history of in utero exposure to ATACAND HCT:
If oliguria or hypotension occurs, direct attention toward support of blood pressure and renal perfusion. Exchange transfusions or dialysis may be required as a means of reversing hypotension and/or substituting for disordered renal function.
Safety and effectiveness in pediatric patients have not been established.
What are the side effects of ATACAND HCT?
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What should I look out for while using ATACAND HCT?
ATACAND HCT is contraindicated in patients who are hypersensitive to candesartan, to hydrochlorothiazide or to other sulfonamide-derived drugs.
Do not co-administer aliskiren with ATACAND HCT in patients with diabetes (see ).
ATACAND HCT is contraindicated in patients with anuria.
What might happen if I take too much ATACAND HCT?
Candesartan Cilexetil-Hydrochlorothiazide
No lethality was observed in acute toxicity studies in mice, rats and dogs given single oral doses of up to 2000 mg/kg of candesartan cilexetil or in rats given single oral doses of up to 2000 mg/kg of candesartan cilexetil in combination with 1000 mg/kg of hydrochlorothiazide. In mice given single oral doses of the primary metabolite, candesartan, the minimum lethal dose was greater than 1000 mg/kg but less than 2000 mg/kg.
Limited data are available in regard to overdosage with candesartan cilexetil in humans. The most likely manifestations of overdosage with candesartan cilexetil would be hypotension, dizziness, and tachycardia; bradycardia could occur from parasympathetic (vagal) stimulation. If symptomatic hypotension should occur, supportive treatment should be initiated. For hydrochlorothiazide, the most common signs and symptoms observed are those caused by electrolyte depletion (hypokalemia, hypochloremia, hyponatremia) and dehydration resulting from excessive diuresis. If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias.
Candesartan cannot be removed by hemodialysis. The degree to which hydrochlorothiazide is removed by hemodialysis has not been established.
Treatment
To obtain up-to-date information about the treatment of overdose, consult your Regional Poison Control Center. Telephone numbers of certified poison control centers are listed in the . In managing overdose, consider the possibilities of multiple-drug overdoses, drug-drug interactions, and altered pharmacokinetics in your patient.
How should I store and handle ATACAND HCT?
Store atNo. 3825 — Tablets ATACAND HCT 16-12.5, are peach, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACS on one side. They are supplied as follows: NDCNo. 3826 — Tablets ATACAND HCT 32-12.5, are yellow, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACJ on one side. They are supplied as follows: NDC No. 3899 — Tablets ATACAND HCT 32–25, are pink, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACD on one side. They are supplied as follows:NDCNo. 3825 — Tablets ATACAND HCT 16-12.5, are peach, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACS on one side. They are supplied as follows: NDCNo. 3826 — Tablets ATACAND HCT 32-12.5, are yellow, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACJ on one side. They are supplied as follows: NDC No. 3899 — Tablets ATACAND HCT 32–25, are pink, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACD on one side. They are supplied as follows:NDCNo. 3825 — Tablets ATACAND HCT 16-12.5, are peach, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACS on one side. They are supplied as follows: NDCNo. 3826 — Tablets ATACAND HCT 32-12.5, are yellow, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACJ on one side. They are supplied as follows: NDC No. 3899 — Tablets ATACAND HCT 32–25, are pink, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACD on one side. They are supplied as follows:NDCNo. 3825 — Tablets ATACAND HCT 16-12.5, are peach, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACS on one side. They are supplied as follows: NDCNo. 3826 — Tablets ATACAND HCT 32-12.5, are yellow, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACJ on one side. They are supplied as follows: NDC No. 3899 — Tablets ATACAND HCT 32–25, are pink, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACD on one side. They are supplied as follows:NDCNo. 3825 — Tablets ATACAND HCT 16-12.5, are peach, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACS on one side. They are supplied as follows: NDCNo. 3826 — Tablets ATACAND HCT 32-12.5, are yellow, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACJ on one side. They are supplied as follows: NDC No. 3899 — Tablets ATACAND HCT 32–25, are pink, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACD on one side. They are supplied as follows:NDCNo. 3825 — Tablets ATACAND HCT 16-12.5, are peach, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACS on one side. They are supplied as follows: NDCNo. 3826 — Tablets ATACAND HCT 32-12.5, are yellow, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACJ on one side. They are supplied as follows: NDC No. 3899 — Tablets ATACAND HCT 32–25, are pink, oval, biconvex, non-film-coated tablets, scored on both sides and coded with ACD on one side. They are supplied as follows:NDC
Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Candesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is, therefore, independent of the pathways for angiotensin II synthesis.
There is also an AT receptor found in many tissues, but AT is not known to be associated with cardiovascular homeostasis. Candesartan has much greater affinity (>10,000-fold) for the AT receptor than for the AT receptor.
Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because candesartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Candesartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.
Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of candesartan on blood pressure.
Hydrochlorothiazide is a thiazide diuretic. Thiazides affect the renal tubular mechanisms of electrolyte reabsorption, directly increasing excretion of sodium and chloride in approximately equivalent amounts. Indirectly, the diuretic action of hydrochlorothiazide reduces plasma volume, with consequent increases in plasma renin activity, increases in aldosterone secretion, increases in urinary potassium loss, and decreases in serum potassium. The renin-aldosterone link is mediated by angiotensin II, so co‑administration of an angiotensin II receptor antagonist tends to reverse the potassium loss associated with these diuretics.
The mechanism of the antihypertensive effect of thiazides is unknown.
Non-Clinical Toxicology
ATACAND HCT is contraindicated in patients who are hypersensitive to candesartan, to hydrochlorothiazide or to other sulfonamide-derived drugs.Do not co-administer aliskiren with ATACAND HCT in patients with diabetes (see ).
ATACAND HCT is contraindicated in patients with anuria.
Because candesartan is not significantly metabolized by the cytochrome P450 system and at therapeutic concentrations has no effects on P450 enzymes, interactions with drugs that inhibit or are metabolized by those enzymes would not be expected.
Non-Steroidal Anti-Inflammatory Agents including Selective Cyclooxygenase-2 Inhibitors (COX-2 Inhibitors)
The antihypertensive effect of angiotensin II receptor antagonists, including candesartan may be attenuated by NSAIDs including selective COX-2 inhibitors.
Lithium
Dual Blockade of the Renin-Angiotensin System (RAS)
Dual blockade of the RAS with angiotensin receptor blockers, ACE inhibitors, or aliskiren is associated with increased risks of hypotension, hyperkalemia, and changes in renal function (including acute renal failure) compared to monotherapy. Closely monitor blood pressure, renal function and electrolytes in patients on ATACAND HCT and other agents that affect the RAS.
Co-administration of ATACAND HCT with potassium sparing diuretics, potassium supplements, potassium-containing salt substitutes or other drugs that raise serum potassium levels may result in hyperkalemia. Monitor serum potassium in such patients.
Do not co-administer aliskiren with ATACAND HCT in patients with diabetes. Avoid use of aliskiren with ATACAND HCT in patients with renal impairment (GFR <60 ml/min) (see ).
Alcohol, barbiturates, or narcotics − Potentiation of orthostatic hypotension may occur.
Antidiabetic drugs (oral agents and insulin) − Dosage adjustment of the antidiabetic drug may be required. Diazoxide − the hyperglycemic effect of diazoxide may be enhanced by thiazides.
Ion Exchange resins − Single doses of either cholestyramine or colestipol resins bind the hydrochlorothiazide and reduce its absorption from the gastrointestinal tract by up to 85% and 43%, respectively. Stagger the dosage of hydrochlorothiazide and ion exchange resins such that hydrochlorothiazide is administered at least 4 hours before or 4-6 hours after the administration of resins.
Skeletal muscle relaxants, nondepolarizing (e.g., tubocurarine) − Possible increased responsiveness to muscle relaxants such as curare derivatives.
Digitalis − Thiazide-induced hypokalemia or hypomagnesemia may predispose to digoxin toxicity. Noradrenaline – Thiazides may decrease arterial responsiveness to noradrenaline, but not enough to preclude effectiveness of the pressor agent for therapeutic use.
Steroids or Adrenocorticotropic Hormone – Hypokalemia may develop during concomitant use of steroids or adrenocorticotropic hormone (ACTH).
Cytotoxic products – Thiazides may reduce the renal excretion of cytotoxic medicinal products (e.g. cyclophosphamide, methotrexate) and potentiate their myelosuppressive effects.
Cyclosporine − Concomitant treatment with cyclosporine may increase the risk of hyperuricemia and gout-type complications.
Hydrochlorothiazide may alter glucose tolerance and raise serum levels of cholesterol and triglycerides.
Hydrochlorothiazide may raise the serum uric acid level due to reduced clearance of uric acid and may cause or exacerbate hyperuricemia and precipitate gout in susceptible patients.
Thiazides decrease urinary calcium excretion and may cause elevation of serum calcium. Avoid using ATACAND HCT in patients with hypercalcemia.
Systemic Lupus Erythematosus
Thiazide diuretics have been reported to cause exacerbation or activation of systemic lupus erythematosus.
Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
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