Norethindrone Acetate and Ethinyl Estradiol

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Overview

What is Norethindrone Acetate and Ethinyl Estradiol?

Norethindrone Acetate and Ethinyl Estradiol Tablets USP is a continuous dosage regimen of a progestin-estrogen combination for oral administration.

The following two strengths of Norethindrone Acetate and Ethinyl Estradiol Tablets USP are available as:

Norethindrone Acetate and Ethinyl Estradiol Tablets USP (0.5 mg/2.5 mcg): Each round, pink to light pink tablet contains 0.5 mg norethindrone acetate, USP and 2.5 mcg ethinyl estradiol, USP.

Norethindrone Acetate and Ethinyl Estradiol Tablets USP (1 mg/5 mcg): Each round, white to off-white tablet contains 1 mg norethindrone acetate, USP and 5 mcg ethinyl estradiol, USP.

Each tablet also contains the following inactive ingredients: calcium stearate, cornstarch, isopropyl alcohol, lactose monohydrate, microcrystalline cellulose, povidone and vitamin E and talc. The 0.5 mg/2.5 mcg pink tablet also contains D&C red no. 30.

The structural formulas are as follows:

Ethinyl Estradiol USP [19-Nor-17α-pregna-1,3,5(10)-trien-20-yne-3,17-diol]

Molecular Weight: 296.40

Molecular Formula: CHO

Norethindrone Acetate USP [19-Norpregn-4-en-20-yn-3-one, 17-(acetyloxy)-, (17 α)]

Molecular Weight: 340.46

Molecular Formula: CHO

What does Norethindrone Acetate and Ethinyl Estradiol look like?

What are the available doses of Norethindrone Acetate and Ethinyl Estradiol?

The following two strengths of Norethindrone Acetate and Ethinyl Estradiol Tablets USP are available:

Norethindrone Acetate and Ethinyl Estradiol TabletsUSP(0.5 mg/2.5 mcg):

Norethindrone Acetate and Ethinyl Estradiol Tablets USP (1 mg/5 mcg):

What should I talk to my health care provider before I take Norethindrone Acetate and Ethinyl Estradiol?

How should I use Norethindrone Acetate and Ethinyl Estradiol?

Norethindrone acetate and ethinyl estradiol tablets are an estrogen plus progestin indicated in a woman with a uterus for:

Use of estrogen-alone, or in combination with a progestin, should be with the lowest effective dose and for the shortest duration consistent with treatment goals and risks for the individual woman. Postmenopausal women should be re-evaluated periodically as clinically appropriate to determine if treatment is still necessary.

What interacts with Norethindrone Acetate and Ethinyl Estradiol?

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What are the warnings of Norethindrone Acetate and Ethinyl Estradiol?

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What are the precautions of Norethindrone Acetate and Ethinyl Estradiol?

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What are the side effects of Norethindrone Acetate and Ethinyl Estradiol?

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What should I look out for while using Norethindrone Acetate and Ethinyl Estradiol?

Norethindrone acetate and ethinyl estradiol tablets are contraindicated in women with any of the following conditions:

What might happen if I take too much Norethindrone Acetate and Ethinyl Estradiol?

Overdosage of estrogen plus progestin may cause nausea, vomiting, breast tenderness, abdominal pain, drowsiness and fatigue, and withdrawal bleeding may occur in women. Treatment of overdose consists of discontinuation of norethindrone acetate and ethinyl estradiol tablets with institution of appropriate symptomatic care.

How should I store and handle Norethindrone Acetate and Ethinyl Estradiol?

StorageStore at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F) [See USP Controlled Room Temperature].StorageStore at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F) [See USP Controlled Room Temperature].Product: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLEProduct: 71335-0516NDC: 71335-0516-0 56 TABLET in a BOTTLENDC: 71335-0516-6 84 TABLET in a BOTTLENDC: 71335-0516-3 60 TABLET in a BOTTLENDC: 71335-0516-9 120 TABLET in a BOTTLENDC: 71335-0516-4 20 TABLET in a BOTTLENDC: 71335-0516-1 14 TABLET in a BOTTLENDC: 71335-0516-7 90 TABLET in a BOTTLENDC: 71335-0516-2 28 TABLET in a BOTTLENDC: 71335-0516-8 100 TABLET in a BOTTLENDC: 71335-0516-5 30 TABLET in a BOTTLE

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Clinical Information

Chemical Structure

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Clinical Pharmacology

Endogenous estrogens are largely responsible for the development and maintenance of the female reproductive system and secondary sexual characteristics. Although circulating estrogens exist in a dynamic equilibrium of metabolic interconversions, estradiol is the principal intracellular human estrogen and is substantially more potent than its metabolites, estrone and estriol, at the receptor level.

The primary source of estrogen in normally cycling adult women is the ovarian follicle, which secretes 70 to 500 mcg of estradiol daily, depending on the phase of the menstrual cycle. After menopause, most endogenous estrogen is produced by conversion of androstenedione, which is secreted by the adrenal cortex, to estrone in the peripheral tissues. Thus, estrone and the sulfate conjugated form, estrone sulfate, are the most abundant circulating estrogens in postmenopausal women. The pharmacologic effects of ethinyl estradiol are similar to those of endogenous estrogens.

Estrogens act through binding to nuclear receptors in estrogen-responsive tissues. To date, two estrogen receptors have been identified. These vary in proportion from tissue to tissue.

Circulating estrogens modulate the pituitary secretion of the gonadotropins, luteinizing hormone (LH) and FSH through a negative feedback mechanism. Estrogens act to reduce the elevated levels of these hormones seen in postmenopausal women.

Progestin compounds enhance cellular differentiation and generally oppose the actions of estrogens by decreasing estrogen receptor levels, increasing local metabolism of estrogens to less active metabolites, or inducing gene products that blunt cellular responses to estrogen. Progestins exert their effects in target cells by binding to specific progesterone receptors that interact with progesterone response elements in target genes. Progesterone receptors have been identified in the female reproductive tract, breast, pituitary, hypothalamus, bone, skeletal tissue and central nervous system. Progestins produce similar endometrial changes to those of the naturally occurring hormone progesterone.

Non-Clinical Toxicology

Norethindrone acetate and ethinyl estradiol tablets are contraindicated in women with any of the following conditions:

Catecholamine-depleting drugs (e.g., reserpine) may have an additive effect when given with beta-blocking agents. Patients treated with atenolol plus a catecholamine depletor should therefore be closely observed for evidence of hypotension and/or marked bradycardia which may produce vertigo, syncope, or postural hypotension.

Calcium channel blockers may also have an additive effect when given with atenolol (see ).

Disopyramide is a Type I antiarrhythmic drug with potent negative inotropic and chronotropic effects. Disopyramide has been associated with severe bradycardia, asystole and heart failure when administered with beta blockers.

Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with beta blockers.

Beta blockers may exacerbate the rebound hypertension which can follow the withdrawal of clonidine. If the two drugs are coadministered, the beta blocker should be withdrawn several days before the gradual withdrawal of clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta blockers should be delayed for several days after clonidine administration has stopped.

Concomitant use of prostaglandin synthase inhibiting drugs, e.g., indomethacin, may decrease the hypotensive effects of beta blockers.

Information on concurrent usage of atenolol and aspirin is limited. Data from several studies, i.e., TIMI-II, ISIS-2, currently do not suggest any clinical interaction between aspirin and beta blockers in the acute myocardial infarction setting.

While taking beta blockers, patients with a history of anaphylactic reaction to a variety of allergens may have a more severe reaction on repeated challenge, either accidental, diagnostic or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat the allergic reaction.

Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia.

An increased risk of PE, DVT, stroke, and MI has been reported with estrogen plus progestin therapy. An increased risk of stroke and DVT has been reported with estrogen-alone therapy. Should any of these occur or be suspected, estrogen with or without progestin therapy should be discontinued immediately.

Risk factors for arterial vascular disease (for example, hypertension, diabetes mellitus, tobacco use, hypercholesterolemia, and obesity) and/or venous thromboembolism (VTE) (for example, personal history or family history of VTE, obesity, and systemic lupus erythematosus) should be managed appropriately.

Stroke

In the WHI estrogen plus progestin substudy, a statistically significant increased risk of stroke was reported in women 50 to 79 years of age receiving daily CE (0.625 mg) plus MPA (2.5 mg) compared to women in the same age group receiving placebo (33 versus 25 per 10,000 women- years) . The increase in risk was demonstrated after the first year and persisted. Should a stroke occur or be suspected, estrogen plus progestin therapy should be discontinued immediately.

In the WHI estrogen-alone substudy, a statistically significant increased risk of stroke was reported in women 50 to 79 years of age receiving daily conjugated estrogens CE (0.625 mg)-alone compared to women in the same age group receiving placebo (45 versus 33 per 10,000 women-years). The increase in risk was demonstrated in year 1 and persisted . Should a stroke occur or be suspected, estrogen-alone therapy should be discontinued immediately.

Subgroup analyses of women 50 to 59 years of age suggest no increased risk of stroke for those women receiving CE (0.625 mg)-alone versus those receiving placebo (18 versus 21 per 10,000 women-years).

Coronary Heart Disease

In the WHI estrogen plus progestin substudy, there was a statistically non-significant increased risk of coronary heart disease (CHD) events (defined as nonfatal MI, silent MI, or CHD death) reported in women receiving daily CE (0.625 mg) plus MPA (2.5 mg) compared to women receiving placebo (41 versus 34 per 10,000 women-years). An increase in relative risk was demonstrated in year 1, and a trend toward decreasing relative risk was reported in years 2 through 5

In the WHI estrogen-alone substudy, no overall effect on CHD events was reported in women receiving estrogen-alone compared to placebo

Subgroup analyses of women 50 to 59 years of age suggest a statistically non-significant reduction in CHD events (CE [0.625 mg]-alone compared to placebo) in women with less than 10 years since menopause (8 versus 16 per 10,000 woman-years).

In postmenopausal women with documented heart disease (n = 2,763), average 66.7 years of age, in a controlled clinical trial of secondary prevention of cardiovascular disease (Heart and Estrogen/Progestin Replacement Study [HERS]), treatment with daily CE (0.625 mg) plus MPA (2.5 mg) demonstrated no cardiovascular benefit. During an average follow-up of 4.1 years, treatment with CE plus MPA did not reduce the overall rate of CHD events in postmenopausal women with established CHD. There were more CHD events in the CE plus MPA-treated group than in the placebo group in year 1, but not during the subsequent years. Two thousand, three hundred and twenty-one (2,321) women from the original HERS trial agreed to participate in an open label extension of HERS, HERS II. Average follow-up in HERS II was an additional 2.7 years, for a total of 6.8 years overall. Rates of CHD events were comparable among women in the CE plus MPA group and the placebo group in HERS, HERS II, and overall.

Venous Thromboembolism

In the WHI estrogen plus progestin substudy, a statistically significant 2-fold greater rate of VTE (DVT and PE) was reported in women receiving daily CE (0.625 mg) plus MPA (2.5 mg) compared to women receiving placebo (35 versus 17 per 10,000 women-years). Statistically significant increases in risk for both DVT (26 versus 13 per 10,000 women-years) and PE (18 versus 8 per 10,000 women-years) were also demonstrated. The increase in VTE risk was demonstrated during the first year and persisted . Should a VTE occur or be suspected, estrogen plus progestin therapy should be discontinued immediately.

In the WHI estrogen-alone substudy, the risk of VTE was increased for women receiving daily CE (0.625 mg)-alone compared to placebo (30 versus 22 per 10,000 women-years), although only the increased risk of DVT reached statistical significance (23 versus 15 per 10,000 women-years). The increase in VTE risk was demonstrated during the first 2 years . Should a VTE occur or be suspected, estrogen-alone therapy should be discontinued immediately.

If feasible, estrogens should be discontinued at least 4 to 6 weeks before surgery of the type associated with an increased risk of thromboembolism or during periods of prolonged immobilization.

The following serious adverse reactions are discussed elsewhere in the labeling:

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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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Professional

Clonazepam Description Each single-scored tablet, for oral administration, contains 0.5 mg, 1 mg, or 2 mg Clonazepam, USP, a benzodiazepine. Each tablet also contains corn starch, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and povidone. Clonazepam tablets USP 0.5 mg contain Yellow D&C No. 10 Aluminum Lake. Clonazepam tablets USP 1 mg contain Yellow D&C No. 10 Aluminum Lake, as well as FD&C Blue No. 1 Aluminum Lake. Chemically, Clonazepam, USP is 5-(o-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has the following structural formula: C15H10ClN3O3 M.W. 315.72

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Interactions

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