Raloxifene Teva: Uses, Dosage & Side Effects

What Is Raloxifene Teva and What Is It Used For?

Raloxifene Teva contains the active substance raloxifene hydrochloride, a second-generation selective estrogen receptor modulator (SERM) manufactured by Teva Pharmaceuticals. As a generic medicine, Raloxifene Teva has been developed and authorised on the basis of bioequivalence to the originator product containing the same active ingredient. Generic medicines must satisfy strict regulatory standards set by the European Medicines Agency (EMA) and the U.S. Food and Drug Administration (FDA), demonstrating that they deliver the same amount of active ingredient to the bloodstream in the same time frame as the original branded product, and thereby produce equivalent clinical effects.

SERMs are a distinctive class of compounds that interact with intracellular estrogen receptors in target organs. Depending on the specific tissue, SERMs can act either as estrogen agonists (mimicking estrogen) or estrogen antagonists (blocking estrogen). Raloxifene was specifically designed to provide the skeletal benefits of estrogen in postmenopausal women while avoiding the potentially harmful estrogenic effects on the breast and uterus that are associated with traditional hormone replacement therapy (HRT). This tissue-selective mechanism makes raloxifene uniquely positioned for bone-protective therapy in postmenopausal women who are at increased risk for osteoporotic fractures but who are not candidates for systemic estrogen replacement.

The loss of estrogen production after menopause is the primary biological driver of postmenopausal osteoporosis, a condition characterised by progressive loss of bone mineral density (BMD), deterioration of bone microarchitecture, and increased susceptibility to fractures. During the first 5 to 10 years after menopause, women can lose up to 20% of their bone density, with the vertebral bodies of the spine and the proximal femur (hip) being particularly vulnerable. Osteoporosis is often called a “silent disease” because bone loss occurs without symptoms until a fracture occurs. Vertebral compression fractures, hip fractures, and wrist fractures are the most common osteoporotic fractures globally, and they carry substantial morbidity, mortality, and healthcare costs. According to the International Osteoporosis Foundation (IOF), one in three women over the age of 50 will experience an osteoporotic fracture in their lifetime.

Raloxifene exerts its tissue-selective effects through a unique molecular mechanism. When raloxifene binds to the estrogen receptor (ER), it induces a conformational change in the receptor that differs from the conformation produced by estradiol (the body's primary endogenous estrogen). This altered conformation affects which coactivator and corepressor proteins are recruited to the receptor-DNA complex, ultimately determining whether gene transcription is activated or suppressed in a given tissue. In bone tissue, raloxifene acts as an estrogen agonist, activating estrogen-responsive genes that promote osteoblast (bone-forming cell) activity and inhibit osteoclast (bone-resorbing cell) function. This results in decreased bone turnover, increased bone mineral density, and preservation of bone structural integrity. In breast tissue and the uterine endometrium, raloxifene acts as an estrogen antagonist, blocking the proliferative effects of estrogen on these tissues and thereby avoiding the risks of breast and endometrial cancer that are associated with unopposed estrogen therapy.

The clinical efficacy of raloxifene in osteoporosis has been established through several large-scale, randomized, double-blind, placebo-controlled clinical trials. The most important of these is the Multiple Outcomes of Raloxifene Evaluation (MORE) trial, a landmark study that enrolled 7,705 postmenopausal women with osteoporosis across 180 clinical centers in 25 countries. The MORE trial demonstrated that raloxifene 60 mg daily significantly reduced the risk of new vertebral fractures by 30% in women with prevalent vertebral fractures and by 50% in women without prevalent fractures, compared with placebo, over a median treatment period of 36 months. These fracture risk reductions were accompanied by significant increases in BMD at the lumbar spine (2.6% increase) and femoral neck (2.1% increase) compared with placebo.

In addition to its skeletal benefits, the MORE trial revealed an unexpected but clinically important finding: raloxifene significantly reduced the incidence of invasive breast cancer in postmenopausal women. Women treated with raloxifene 60 mg daily had a 72% reduction in the risk of invasive breast cancer compared with the placebo group over 4 years of follow-up. This breast cancer risk reduction was subsequently confirmed and extended in the Raloxifene Use for The Heart (RUTH) trial, a large cardiovascular outcomes study involving 10,101 postmenopausal women at increased risk for major coronary events. The RUTH trial demonstrated a 44% reduction in invasive breast cancer incidence with raloxifene over a median follow-up of 5.6 years, while showing no increase in coronary heart disease events. Because Raloxifene Teva contains the same active ingredient at the same dose, these clinical outcomes apply equally to patients treated with the generic product.

Raloxifene was first approved by the U.S. FDA in December 1997 for the prevention of osteoporosis in postmenopausal women, and its indication was subsequently expanded to include treatment of osteoporosis. The European Medicines Agency (EMA) granted marketing authorization for raloxifene in the European Union in 1998. In 2007, the FDA additionally approved raloxifene for the reduction of risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk for invasive breast cancer. Following patent expiration of the originator product, generic versions such as Raloxifene Teva became available, offering patients and healthcare systems the same clinical benefit at lower cost. Raloxifene-containing medicines are currently approved and marketed in more than 70 countries worldwide.

What Should You Know Before Taking Raloxifene Teva?

Contraindications

Raloxifene Teva must not be used in several clearly defined clinical situations, which are consistent across all raloxifene-containing products. The most critical contraindication is active or past history of venous thromboembolic events (VTE), including deep vein thrombosis (DVT), pulmonary embolism (PE), and retinal vein thrombosis. Raloxifene increases the risk of VTE by approximately 1.5 to 3 times compared with placebo, and this risk is highest during the first 4 months of treatment and during periods of immobilization. In the MORE trial, the incidence of DVT was 1.0% in the raloxifene 60 mg group compared with 0.5% in the placebo group over 3 years. In the RUTH trial, VTE events occurred in 3.1% of raloxifene-treated women compared with 2.0% in the placebo group over 5.6 years.

Additional contraindications include: hypersensitivity to raloxifene or any of the excipients in the Raloxifene Teva formulation; pregnancy or possibility of pregnancy (raloxifene is Pregnancy Category X—it may cause fetal harm); breastfeeding; unexplained uterine bleeding that has not been evaluated by a healthcare provider; any signs or symptoms of endometrial cancer (the safety of raloxifene in this population has not been adequately studied); and severe hepatic impairment, including cholestasis. Raloxifene should also not be used in premenopausal women, as its safety and efficacy have only been established in postmenopausal women.

Warnings and Precautions

Before starting Raloxifene Teva, discuss the following important considerations with your healthcare provider:

• Venous thromboembolism: As described above, raloxifene increases VTE risk. Women with additional risk factors for VTE—such as obesity (BMI > 30), varicose veins, history of superficial thrombophlebitis, active smoking, prolonged immobility, or use of systemic estrogens—should be carefully evaluated before starting treatment. The benefit-risk ratio should be considered individually for each patient, and alternative osteoporosis therapies should be explored when VTE risk is high.
• Stroke risk: In the RUTH trial, raloxifene was associated with an increased risk of fatal stroke compared with placebo (59 versus 39 events; hazard ratio 1.49). This risk increase was primarily observed in women with established cardiovascular risk factors. Women at increased risk for stroke—such as those with a history of stroke or transient ischemic attack, atrial fibrillation, uncontrolled hypertension, or heavy smoking—should discuss the potential stroke risk with their doctor before starting Raloxifene Teva.
• Hepatic impairment: Raloxifene is extensively metabolized in the liver through glucuronidation. It has not been adequately studied in patients with moderate hepatic impairment and is contraindicated in severe hepatic impairment (including cholestatic liver disease). Serum raloxifene concentrations may be elevated in patients with impaired liver function. Liver function tests should be performed before starting treatment and periodically thereafter in patients with any underlying liver disease.
• Renal impairment: Raloxifene Teva should be used with caution in patients with moderate to severe renal impairment. In pharmacokinetic studies, single doses of raloxifene resulted in a 56% higher area under the plasma concentration-time curve (AUC) in patients with mild renal impairment compared with healthy volunteers. The clinical significance of this finding in long-term use is not fully established, but closer monitoring is appropriate in patients with a creatinine clearance below 60 mL/min.
• Triglycerides: Raloxifene has been associated with modest increases in serum triglyceride levels. In clinical trials, serum triglycerides increased by approximately 6–11% compared with placebo. Women with pre-existing hypertriglyceridemia (especially levels greater than 500 mg/dL) should be monitored closely, as substantial triglyceride elevations may increase the risk of pancreatitis. In women with a history of marked hypertriglyceridemia on oral estrogen therapy, raloxifene may produce a similar response.
• Breast abnormalities: Any unexplained breast abnormality that occurs during raloxifene therapy should be investigated. Raloxifene does not eliminate the risk of breast cancer, and women should continue with routine breast cancer screening (mammography and clinical breast examination) according to local guidelines.

Pregnancy and Breastfeeding

Raloxifene Teva is strictly contraindicated during pregnancy and in women who may become pregnant. Raloxifene is classified as Pregnancy Category X, meaning that animal studies have shown evidence of fetal toxicity and the risk to the fetus clearly outweighs any potential benefit. In animal reproductive studies, raloxifene caused delays in fetal development, decreased neonatal survival, altered physical development, changes in reproductive tract development (including feminization of male fetuses), and reduced fertility in offspring. Although Raloxifene Teva is indicated only for postmenopausal women (who cannot become pregnant naturally), any woman of childbearing potential should have a negative pregnancy test before starting treatment, and effective contraception must be used if there is any possibility of pregnancy.

It is not known whether raloxifene is excreted in human breast milk. Given the potential for serious adverse effects on the nursing infant, Raloxifene Teva must not be used during breastfeeding. This contraindication is primarily relevant in the rare clinical scenario where raloxifene might be considered for off-label use in premenopausal women for breast cancer chemoprevention.

Hot Flashes and Menopausal Symptoms

Unlike traditional hormone replacement therapy, Raloxifene Teva does not relieve and may actually worsen vasomotor symptoms (hot flashes and night sweats). In the MORE trial, the incidence of hot flashes was approximately 24.6% in the raloxifene 60 mg group compared with 18.3% in the placebo group. This is an important consideration for women who are still experiencing significant menopausal symptoms at the time of initiating osteoporosis therapy, as raloxifene would not provide symptomatic relief and might increase their discomfort. Women for whom hot flashes are a significant quality-of-life concern should discuss alternative treatment options with their healthcare provider, such as bisphosphonates or denosumab.

Driving and Operating Machinery

Raloxifene Teva is not expected to affect the ability to drive or operate machinery. No specific studies on driving ability have been performed with raloxifene. Based on its pharmacological profile and the side effects observed in clinical trials, raloxifene does not cause sedation, dizziness, or impairment of cognitive function that would interfere with driving or operating machinery. However, individual responses to any medication can vary, and patients should exercise appropriate caution when starting treatment, particularly if they experience any new symptoms such as dizziness or visual disturbances.

How Does Raloxifene Teva Interact with Other Drugs?

Raloxifene is extensively metabolized through glucuronidation in the gut wall and liver, primarily by uridine diphosphate-glucuronosyltransferase (UGT) enzymes. Unlike many oral medications, raloxifene does not undergo significant cytochrome P450 (CYP) enzyme-mediated metabolism. This distinct metabolic pathway means that classic CYP-mediated drug interactions are generally not a concern with Raloxifene Teva. However, the glucuronidation pathway, the drug's high plasma protein binding, and its enterohepatic recirculation create specific interaction risks that are clinically relevant and must be considered when prescribing raloxifene alongside other medications.

Raloxifene is more than 95% bound to plasma proteins, including albumin and alpha-1 acid glycoprotein. It does not, however, appear to interact with the binding of other highly protein-bound drugs such as warfarin, phenytoin, or tamoxifen in clinical studies, although interactions at the pharmacodynamic level may occur with some of these agents. The following table summarises the most clinically relevant interactions to be aware of when taking Raloxifene Teva.

Major Interactions

The most clinically significant interaction is between raloxifene and cholestyramine (and by extension, other bile acid sequestrants such as colestipol and colesevelam). Cholestyramine reduces the absorption and enterohepatic cycling of raloxifene by approximately 60%, which substantially diminishes the drug's therapeutic effect. Raloxifene undergoes significant enterohepatic recirculation—after oral administration, it is absorbed, conjugated to glucuronides in the gut wall and liver, excreted in bile, hydrolyzed back to raloxifene by gut bacteria, and reabsorbed. Bile acid sequestrants interrupt this recycling process by binding to the glucuronide conjugates in the gut, preventing their reabsorption. If both medications are absolutely necessary, they should be separated by at least 4 to 6 hours, although avoidance of concomitant use is preferred.

The interaction between raloxifene and warfarin is also clinically important. In clinical studies, raloxifene has been shown to produce a modest (approximately 10%) decrease in prothrombin time when given concomitantly with warfarin. While this effect is relatively small, the narrow therapeutic index of warfarin means that even modest changes in anticoagulant activity can have clinically meaningful consequences. The international normalized ratio (INR) should therefore be monitored closely when Raloxifene Teva therapy is initiated, changed, or discontinued in patients taking warfarin or other vitamin K antagonists. The same general principle of monitoring coagulation status is advised for other oral anticoagulants, although direct data are limited.

Concomitant use of raloxifene with systemic estrogens (such as oral estradiol, conjugated estrogens, or transdermal estrogen patches) has not been studied in clinical trials, and the safety and efficacy of this combination have not been established. Because raloxifene can act as a partial estrogen antagonist on some tissues, combining it with systemic estrogen therapy could theoretically reduce the effectiveness of both agents and complicate the overall benefit-risk profile. Raloxifene Teva and systemic estrogens should therefore not be used together; the choice between the two should be made based on the patient's specific clinical situation and therapeutic goals.

Minor Interactions

Ampicillin reduces the peak plasma concentration of raloxifene by approximately 28%, likely by altering intestinal bacteria involved in the enterohepatic recycling of raloxifene glucuronides. However, the overall extent of absorption (as measured by AUC) is not significantly affected, and this interaction is not considered clinically significant. No dosage adjustment is required when Raloxifene Teva is taken with ampicillin or other antibiotics. Nonetheless, if long-term antibiotic therapy is planned, the prescriber may wish to consider the overall therapeutic strategy.

Raloxifene does not affect the pharmacokinetics of methylprednisolone given as a single intravenous dose. Additionally, population pharmacokinetic analyses from clinical trials have shown that commonly co-administered medications—including calcium supplements, vitamin D supplements, acetaminophen (paracetamol), nonsteroidal anti-inflammatory drugs (NSAIDs), oral hypoglycemics, proton pump inhibitors, and H2-receptor antagonists—do not significantly affect raloxifene plasma concentrations. Digoxin pharmacokinetics are also not affected by raloxifene, which is reassuring for older patients who may be taking cardiac medications.

What Is the Correct Dosage of Raloxifene Teva?

Adults (Postmenopausal Women)

The duration of treatment with Raloxifene Teva should be individualized based on the patient's fracture risk, response to therapy, and ongoing benefit-risk assessment. In clinical trials, the efficacy and safety of raloxifene have been demonstrated over treatment periods of up to 8 years (the original 4-year MORE trial plus a 4-year extension study, known as CORE—Continuing Outcomes Relevant to Evista). Current clinical guidelines from NOF, IOF, and NICE generally recommend that osteoporosis treatment be continued for at least 3 to 5 years, with reassessment of the need for ongoing therapy at regular intervals. Unlike bisphosphonates, there is no concern about a prolonged skeletal half-life with raloxifene, meaning that the drug does not accumulate in bone and its effects are reversible upon discontinuation. When raloxifene is stopped, bone mineral density returns toward pre-treatment levels over 1 to 2 years.

Children and Adolescents

Raloxifene Teva is not indicated for use in children, adolescents, or premenopausal women. The safety and efficacy of raloxifene have not been established in pediatric populations, and raloxifene is known to interfere with normal reproductive tract development. Osteoporosis treatment in children and adolescents (for example, secondary to long-term glucocorticoid therapy, chronic inflammatory conditions, or genetic disorders such as osteogenesis imperfecta) requires different therapeutic approaches. Healthcare providers should consider age-appropriate alternatives such as bisphosphonates with appropriate pediatric dosing, typically under the supervision of a pediatric endocrinologist or metabolic bone specialist.

Elderly Patients

No dose adjustment is required for elderly postmenopausal women taking Raloxifene Teva. In clinical trials, the majority of participants were 65 years of age or older, and raloxifene demonstrated consistent efficacy in reducing vertebral fracture risk across all age subgroups studied (up to age 80). The pharmacokinetics of raloxifene are not significantly altered by age alone. However, elderly patients may have additional risk factors for venous thromboembolism, including decreased mobility, concurrent medications (such as diuretics or anticholinergic drugs), and comorbid conditions. The benefit-risk assessment should therefore be considered carefully in this population, and elderly patients should be counselled about the importance of staying mobile and recognising early signs of VTE.

Missed Dose

If you miss a dose of Raloxifene Teva, take it as soon as you remember on the same day. If it is already the next day, skip the missed dose and take the next dose at your usual time. Do not take a double dose to make up for a missed dose. The long elimination half-life of raloxifene (approximately 27.7 hours) means that a single missed dose is unlikely to significantly affect the overall therapeutic effect. However, consistent daily adherence is important for optimal long-term bone protection. Setting a daily phone alarm, using a pill organiser, or associating the tablet with a regular daily activity (such as breakfast or brushing teeth) can help improve adherence over months and years of therapy.

Overdose

There is limited clinical experience with raloxifene overdose. In clinical trials, doses up to 600 mg/day (10 times the recommended dose) were administered for 8 weeks without dose-limiting adverse effects. In a post-marketing surveillance study, an adult ingested 1,500 mg of raloxifene and recovered without sequelae. There is no specific antidote for raloxifene overdose. Treatment should be supportive and symptomatic, focusing on airway protection, circulatory support, and monitoring for signs of venous thromboembolism in the event of large overdoses. Symptoms that might be expected based on the pharmacological profile include leg cramps, dizziness, hot flashes, nausea, and vomiting. In the event of a suspected overdose of Raloxifene Teva, contact your local poison control center or emergency department immediately. Activated charcoal may be considered for recent ingestions if the patient presents within 1 hour.

What Are the Side Effects of Raloxifene Teva?

Like all medicines, Raloxifene Teva can cause side effects, although not everybody gets them. The safety profile of raloxifene has been extensively characterized through large clinical trials involving more than 25,000 postmenopausal women, with follow-up periods extending up to 8 years. The overall discontinuation rate due to adverse events in clinical trials was similar between the raloxifene and placebo groups, indicating that the medication is generally well tolerated. Because Raloxifene Teva is therapeutically equivalent to the originator product, the side-effect profile is identical. The side effects below are categorized by frequency according to the standard medical classification system used in the EMA Summary of Product Characteristics.

The most clinically important adverse effect of Raloxifene Teva is the increased risk of venous thromboembolism (VTE). In the MORE trial, the incidence of VTE (DVT and PE combined) was approximately 1.0% in the raloxifene group compared with 0.3% in the placebo group over 40 months. In the RUTH trial, VTE occurred in 3.1% of raloxifene-treated women compared with 2.0% in the placebo group over 5.6 years. The absolute risk is relatively low in an average patient, but women with additional VTE risk factors should be carefully assessed before starting treatment. Warning signs of VTE include sudden pain, swelling, or warmth in one leg (suggesting DVT), or sudden shortness of breath, chest pain, or coughing up blood (suggesting PE), and require immediate medical attention. The risk of VTE is particularly elevated during the first 4 months of treatment and during any period of prolonged immobilization.

Hot flashes are the most common reason patients discontinue raloxifene therapy. They tend to be most pronounced during the first 6 months of therapy and generally improve over time as the body adapts. In clinical trials, about 24.6% of raloxifene-treated women reported hot flashes compared with 18.3% in the placebo group. The mechanism is related to raloxifene's partial antagonist activity at estrogen receptors in the thermoregulatory center of the hypothalamus. Hot flashes are more common in women who experienced significant menopausal vasomotor symptoms before starting treatment, and in women who started raloxifene early in menopause when endogenous estrogen levels were still fluctuating.

Leg cramps are another frequently reported side effect, occurring in approximately 5.9% to 9.2% of raloxifene-treated women compared with 3.7% to 6.0% in placebo groups. The exact mechanism is not fully understood but may relate to raloxifene's effects on calcium homeostasis, magnesium metabolism, or vascular smooth muscle. Leg cramps are usually mild to moderate in severity and can often be managed with stretching exercises, adequate hydration, and ensuring sufficient magnesium and potassium intake through diet or supplementation. Severe or persistent leg cramps should be evaluated to rule out DVT.

Importantly, Raloxifene Teva has a favorable safety profile compared with traditional hormone replacement therapy regarding certain outcomes. Unlike combined estrogen-progestin HRT, raloxifene does not cause breast tenderness, uterine bleeding, or endometrial hyperplasia. It does not increase the risk of endometrial cancer, which is a concern with unopposed estrogen therapy. The MORE trial and its extension studies (including CORE) demonstrated a significant reduction in the incidence of invasive breast cancer with raloxifene treatment. Additionally, raloxifene has beneficial effects on several cardiovascular risk markers, including reductions in total cholesterol and LDL cholesterol of around 7% and 12% respectively, without significantly affecting HDL cholesterol or triglyceride levels in most patients, although modest triglyceride increases have been reported in some women.

If you experience side effects, discuss them with your doctor or pharmacist. Many side effects are mild and resolve with time, but any new or worsening symptom should be reported. In the European Union, suspected adverse reactions can be reported via the national reporting system (such as the UK's Yellow Card Scheme, the Swedish Medical Products Agency, or equivalent bodies), which helps regulators continue to monitor the safety of medicines. In the United States, suspected adverse reactions can be reported to FDA MedWatch.

How Should You Store Raloxifene Teva?

Proper storage of Raloxifene Teva is important to ensure that the medication remains effective and safe throughout its shelf life, which is typically 3 years from the date of manufacture. The following storage guidelines should be followed by all patients:

• Temperature: Store at room temperature, not above 25°C (77°F). Do not freeze. Brief exposure to temperatures up to 30°C (86°F) during transportation or warmer weather is acceptable but should be minimized. Avoid storing the medication in locations subject to significant temperature fluctuations, such as near radiators, windows in direct sunlight, or inside a car.
• Light protection: Keep the tablets in their original blister packaging until ready to use, as raloxifene may be sensitive to prolonged light exposure. Do not transfer tablets to other containers such as weekly pill organisers for extended periods.
• Moisture: Store in a dry place. Do not store in the bathroom or other areas with high humidity, as moisture can degrade the film coating and potentially affect the stability of the active ingredient.
• Children: Keep out of reach and sight of children. Store in a secure location to prevent accidental ingestion. Raloxifene can cause serious harm to developing fetuses and should not be handled by pregnant women (other than the patient herself).
• Expiration date: Do not use Raloxifene Teva after the expiration date (EXP) printed on the blister pack and carton. The expiration date refers to the last day of that month. Expired medication may have reduced potency and should not be taken.
• Tablet appearance: If you notice any change in the appearance of the tablets (such as discoloration, crumbling, unusual odor, or a damaged blister), do not take them and consult your pharmacist.

Do not dispose of unused or expired medications in household waste, down the drain, or in the toilet. Pharmaceutical residues in wastewater can contribute to environmental contamination and may ultimately affect aquatic wildlife and drinking water sources. Return unused or expired tablets in their original packaging to your pharmacist or local medicine take-back programme for safe disposal. Most pharmacies across Europe, the UK, and North America offer free medicine return schemes in line with environmental regulations. These measures help protect the environment while ensuring that prescription medicines do not enter circulation outside of proper medical supervision.

What Does Raloxifene Teva Contain?

Active ingredient: Each film-coated tablet of Raloxifene Teva contains raloxifene hydrochloride 60 mg, which is equivalent to approximately 56 mg of raloxifene free base. Raloxifene hydrochloride has the molecular formula C₂₈H₂₇NO₄S·HCl and a molecular weight of 510.05 g/mol. It is a white to pale yellow solid that is slightly soluble in water. Chemically, raloxifene is a benzothiophene derivative structurally distinct from steroidal estrogens, which contributes to its selective receptor modulator profile.

Inactive ingredients (excipients): The tablet core typically contains povidone, polysorbate 80, lactose monohydrate, lactose anhydrous, crospovidone (a disintegrant), magnesium stearate (a lubricant), and purified water (which is removed during the manufacturing process). The film coating consists of hypromellose, titanium dioxide (E171, a white colouring agent), macrogol (polyethylene glycol), and other pharmaceutically acceptable film-forming agents that give the tablet its characteristic smooth, white to off-white appearance. Exact excipient composition may vary between generic manufacturers and should be confirmed by reading the patient information leaflet that accompanies the pack.

Important note for patients with lactose intolerance: Raloxifene Teva tablets contain lactose (both monohydrate and anhydrous forms). Patients with rare hereditary problems of galactose intolerance, total lactase deficiency, or glucose-galactose malabsorption should not take this medicine. The amount of lactose per tablet is relatively small and is unlikely to cause symptoms in most patients with mild lactose intolerance, but patients with severe lactose intolerance or hereditary metabolic disorders should discuss this with their healthcare provider before starting treatment.

Tablet description: Raloxifene Teva 60 mg film-coated tablets are white to off-white and oval-shaped. The exact imprint and appearance may vary by country and manufacturing site. The tablets are typically packaged in PVC/PVDC/aluminum blister packs, available in pack sizes that commonly include 28, 30, 84, or 90 tablets (not all pack sizes may be marketed in all countries). Always check that the packaging is intact and the tablets match the description before taking the medicine, and consult a pharmacist if anything appears unusual.