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Raloxifene | CAS No: 84449-90-1 | GMP-certified suppliers
A medication that supports prevention and treatment of osteoporosis in postmenopausal women, including steroid‑related bone loss, while also lowering invasive breast cancer risk in eligible patients.
Therapeutic categories
BCRP/ABCG2 SubstratesBenzene DerivativesBenzylidene CompoundsBone Density Conservation AgentsCytochrome P-450 CYP2B6 InhibitorsCytochrome P-450 CYP2B6 Inhibitors (strong)
Generic name
Raloxifene
Molecule type
small molecule
CAS number
84449-90-1
DrugBank ID
DB00481
Approval status
Approved drug, Investigational drug
ATC code
G03XC01
Primary indications
- Indicated for the prevention and treatment of osteoporosis in postmenopausal women, as well as prevention and treatment of corticosteroid-induced bone loss
- [label]
- Indicated for the reduction in the risk of invasive breast cancer in postmenopausal women with osteoporosis or postmenopausal women with a high risk for invasive breast cancer
- [label]
Product Snapshot
- Oral small‑molecule tablets used as the API for solid‑dose formulations
- Primary uses include osteoporosis prevention and treatment in postmenopausal women and reduction of invasive breast cancer risk in defined high‑risk populations
- Approved in the US, EU, and Canada, with some investigational activity noted in additional markets
Clinical Overview
Raloxifene (CAS 84449-90-1) is a second‑generation selective estrogen receptor modulator used for the prevention and treatment of osteoporosis in postmenopausal women, including corticosteroid‑induced bone loss. It is also indicated to reduce the risk of invasive breast cancer in postmenopausal women with osteoporosis or those at high breast cancer risk. It produces estrogen‑agonist activity in bone and lipid metabolism while acting as an estrogen antagonist in breast and uterine tissues. Evista is a widely known brand.
Raloxifene enhances bone mineral density by stimulating osteoblast activity and suppressing osteoclast‑mediated resorption. Clinical trials have demonstrated increases in lumbar spine, hip, femoral neck, and total body bone density, along with reduced vertebral fracture incidence. Short‑term reductions in biochemical markers of bone turnover have also been observed. Antagonism of estrogen receptors in breast tissue contributes to reductions in estrogen receptor‑positive breast cancer risk, although the drug does not treat established breast cancer.
The mechanism of action involves high‑affinity binding to estrogen receptors, inducing tissue‑specific conformational changes that modulate recruitment of coactivators or corepressors. In bone, raloxifene influences transcription through both estrogen response elements and a distinct raloxifene response element, increasing expression of bone matrix proteins. Its antiestrogenic effects in breast tissue reduce proliferative signaling and inflammatory cell recruitment.
Raloxifene undergoes extensive first‑pass metabolism and is primarily glucuronidated, consistent with its classification as a UGT1A1 substrate. It is a substrate for P‑glycoprotein and OATP transporters and has documented inhibitory effects on several CYP isoenzymes. Oral bioavailability is low, and enterohepatic recirculation contributes to a long elimination half‑life.
Safety considerations include a recognized risk of venous thromboembolism. In certain high‑risk populations, an increased incidence of fatal stroke has been reported. It is not associated with endometrial proliferation.
For API procurement, sourcing should ensure control of polymorphic form, impurity profile, and stability under typical storage conditions to support global regulatory submissions.
Raloxifene enhances bone mineral density by stimulating osteoblast activity and suppressing osteoclast‑mediated resorption. Clinical trials have demonstrated increases in lumbar spine, hip, femoral neck, and total body bone density, along with reduced vertebral fracture incidence. Short‑term reductions in biochemical markers of bone turnover have also been observed. Antagonism of estrogen receptors in breast tissue contributes to reductions in estrogen receptor‑positive breast cancer risk, although the drug does not treat established breast cancer.
The mechanism of action involves high‑affinity binding to estrogen receptors, inducing tissue‑specific conformational changes that modulate recruitment of coactivators or corepressors. In bone, raloxifene influences transcription through both estrogen response elements and a distinct raloxifene response element, increasing expression of bone matrix proteins. Its antiestrogenic effects in breast tissue reduce proliferative signaling and inflammatory cell recruitment.
Raloxifene undergoes extensive first‑pass metabolism and is primarily glucuronidated, consistent with its classification as a UGT1A1 substrate. It is a substrate for P‑glycoprotein and OATP transporters and has documented inhibitory effects on several CYP isoenzymes. Oral bioavailability is low, and enterohepatic recirculation contributes to a long elimination half‑life.
Safety considerations include a recognized risk of venous thromboembolism. In certain high‑risk populations, an increased incidence of fatal stroke has been reported. It is not associated with endometrial proliferation.
For API procurement, sourcing should ensure control of polymorphic form, impurity profile, and stability under typical storage conditions to support global regulatory submissions.
Identification & chemistry
| Generic name | Raloxifene |
|---|---|
| Molecule type | Small molecule |
| CAS | 84449-90-1 |
| UNII | YX9162EO3I |
| DrugBank ID | DB00481 |
Pharmacology
| Summary | Raloxifene is a selective estrogen receptor modulator that binds ERα and ERβ, acting as an agonist in bone and lipid pathways while functioning as an antagonist in breast and uterine tissues. Its pharmacologic activity is driven by tissue‑specific recruitment of coactivators and corepressors, leading to modulation of estrogen‑responsive gene transcription. The drug enhances bone matrix protein expression and suppresses estrogen‑dependent cellular proliferation in breast tissue, reflecting its dual estrogenic and anti‑estrogenic profiles. |
|---|---|
| Mechanism of action | Raloxifene is a selective estrogen receptor modulator that acts as both an estrogen agonist and antagonist via differential effects on the tissue-specific estrogen receptors. Based on the findings of competitive binding assays, raloxifene displays binding affinity that is similar to that of [estradiol], the predominant circulating estrogen.Estrogens play variable roles at different tissues in females, including the bone, breasts, uterus and liver, by binding to the steroid nuclear hormone receptors, Estrogen Receptor alpha (ERα) or Estrogen Receptor beta (ERβ).These receptors are normally bound to the Heat Shock Protein 90 (Hsp90) when unbound to the ligand. Ligand binding induces a conformational change in the receptor that promotes dissociation of the receptor from Hsp90, dimerization and translocation into the nucleus. This movement into the nucleus allows the receptor to bind to genomic locations based on sequence recognition of the DNA binding domain, also known as the Estrogen Response Elements (EREs). In bones, endogenous estrogens normally modulate multiple DNA response elements, including the gene-encoding transforming growth factor-β3 (TGF-β3), which is a cytokine embedded in the bone matrix.TGF-β3 plays an important role in bone remodellingby working with other cytokines to induce production of osteoblasts, such as IL-6, and attenuate the activity of osetoclasts. Estrogens typically maintain the bone integrity by inhibiting the cytokines that recruit osteoclasts and oppose the bone-resorbing, Ca2+-mobilizing action of parathyroid hormone. In contrast, estrogens promote osteoblast proliferation, augment the production of TGF-β3 and bone morphogenic proteins, and inhibit apoptosis.Mimicking the action of endogenous estrogen in bone tissues, raloxifene binds to the estrogen receptor to influence gene transcription through interactions with the estrogen response element (ERE) and a distinct DNA target, the raloxifene response element (RRE).It occupies the same ER ligand binding site as estrogen.Upon binding, raloxifene induces a conformational change of the receptor, allowing mediation of direct binding to transcriptional elements by accessory proteins. Increased expression of bone matrix proteins, such as alkaline phosphatase, osteonectin, osteocalcin and collagen may be seen.The agonistic or antagonistic action of raloxifene depends on the extent of recruitment of coactivators and corepressors to estrogen receptor (ER) target gene promotors.[label] In breast tissues, raloxifene acts as an estrogen receptor antagonist to attenuate the estrogen-dependent proliferative effects of epithelial cell expansion. In addition to the antiproliferative effects, raloxifene prevents the production of cytokines and recruitment of macrophages and lymphocytes into tumor mass. |
| Pharmacodynamics | Raloxifene belongs to the selective estrogen receptor modulator (SERM) drug class that exhibits estrogenic effects on bone and lipid metabolism while mediating anti-estrogenic effects on uterine endometrium and breast tissues.On skeletal tissues, raloxifene stimulates bone-depositing osteoblasts and inhibits bone-resorbing osteoclaststo augument bone mineral density.Raloxifene produces estrogen-like effects on bone, reducing the resorption of bone and increasing bone mineral density in postmenopausal women, thus slowing the rate of bone loss.[label] In three randomized, placebo-controlled trials in Europe, postmenopausal women receiving raloxifene at variable doses of 30 to 150 mg daily demonstrated significant increases in bone mineral density in the lumbar spine, total hip, femoral neck and total body compared to placebo.In the MORE and RUTH trials, there were fewer incidences of vertebral fractures in postmeopausal women receiving raloxifene compared to placebo.In a eight-week study evaluating short-term effects of raloxifene in healthy postmenopausal women, there was a decrease in the bone turnover markers, such as serum alkaline phosphatase level, serum osteocalcin level and urinary calcium excretion. Raloxifene was shown to inhibit estrogen-dependent proliferation of human breast cancer cells _in vitro_ and development of induced mammary tumors in rats _in vivo_.In adult female rats, raloxifene produced a greater regression of the mammary gland than [tamoxifen].The MORE trial was a multicenter, randomized, double-blind clinical trial that investigated the long-term effects of the drug therapy in European and American postmenopausal women receiving raloxifene for 40 months.Additionally, a reduction in the incidence of invasive breast cancer was also demonstrates in the CORE and RUTH trials.Study findings demonstrated that compared to placebo, the risk of invasive breast cancer was decreased by 76% among postmenopausal women with osteoporosis. There was a decrease in the risk of estrogen receptor-positive breast cancer by 90% but there was no increase in the risk of endometrial cancer. Unlike hormone replacement therapy, raloxifene does not mediate proliferative or stimulatory effects on endometrial tissue. Findings from both animal and human studies demonstrated no significant changes in the histologic appearance of the endometrium. Raloxifene promotes estrogen-like effects on lipid metabolism. In a European trial that evaluated lipid profiles following raloxifene therapy over the 24-month period, there were significant decreases in the serum concentrations of total and low-density lipoprotein (LDL) cholesterol over a 24-month period of raloxifene therapy.Raloxifene is not associated with causing alterations in the serum levels of HDL cholesterol or triglycerides.As the HDL choesterol level is considered a strong inverse predictor of cardiovascular disease in women, the cardioprotective effects of raloxifene were questioned. Due to limited data on the long-term trials, it is not possible to determine whether the small lipid effects produced by raloxifene correlate with a smaller degree of cardioprotective activity compared with hormone replacement therapy. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Estrogen receptor alpha | Humans | agonist |
| Estrogen receptor beta | Humans | agonist |
| Serpin B9 | Humans |
ADME / PK
| Absorption | Raloxifene is well absorbed from the gastrointestinal tract, with approximately 60% fo the drug being absorbed following oral administration.Due to the extensive first-pass hepatic metabolism that involves glucuronide conjugation, the absolute oral bioavailability of raloxifene is about 2%.Following oral ingestion of a single dose or multiple dose of raloxifen in healthy postmenopausal women, the mean peak plasma concentrations (Cmax) were 0.50 and 1.36 ng/mL, respectively, and the AUC values were 27.2 and 24.2 ngxhr/mL, respectively. The time to reach Cmax following a single or multiple oral doses were 27.7 and 32.5 hours, respectively.[label] Although not clinically significant, oral ingestion of raloxifene with high-fat meals is thought to increase the systemic bioavailability of the drugby increasnig the peak plasma concentrations (Cmax) and AUC by 28% and 16%, respectively.[label] |
|---|---|
| Half-life | The average plasma elimination half-life of raloxifene ranges from 27 to 32 hours.The prolonged half-life has been attributed to the drug's reversible systemic metabolism and significant enterohepatic cycling. |
| Protein binding | About 95% of raloxifene and its glucuronide metabolites are bound to plasma proteins.[label] Although this is a relatively high protein binding profile, _in vitro_ studies suggest that raloxifene and its metabolites do not significantly interact with binding of highly protein-bound drugs.FDA Label still advises patients to use raloxifene with caution co-administering with other highly protein-bound drugs.[label] |
| Metabolism | Raloxifene is reported to undergo metabolism in the intestines and liver devoid of cytochrome P450 pathway.It is extensively metabolized, where less than 1% of the total dose exists as unchanged compound.[label] It mainly undergoes first-pass metabolism to form glucuronide conjugates, raloxifene-4'-glucuronide (raloxifene-4'-β-glucuronide), raloxifene-6-glucuronide (raloxifene-6-β-glucuronide), and raloxifene-6,4'-diglucuronide. No other metabolites have been detected in human plasma. The terminal log-linear portions of the plasma concentration curves for raloxifene and the glucuronides are generally parallel. This is consistent with interconversion of raloxifene and the glucuronide metabolites.[label] |
| Route of elimination | Raloxifene predominantly undergoes fecal excretion, with less than 0.2% of the dose being excreted in the urine as unchanged form of the compound and less than 6% of the dose being excreted as glucuronide conjugates. Co-administration with [cholestyramine], a bile acid sequestrant, was shown to reduce the enterohepatic recycling of raloxifene by 60%. |
| Volume of distribution | Following oral administration of single doses randing from 30 to 150 mg in postmenopausal women, the volume of distribution was about 2348 L/kg. Following oral administration of multiple doses, the value increased to 2853 L/kg. Raloxifene is widely distributed in the tissues. It is not known whether raloxifene is excreted in human milk.[label] |
| Clearance | Following intravenous administration, raloxifene was shown to be cleared at a rate approximating hepatic blood flow. The apparent oral clearance is reported to be 44.1 L/kgxhr. The clearance can range from 40 to 60L/kgxhr following chronic dosing. In healthy postmenopausal women receiving multiple oral dose, the mean clearance was 47.4 L/kgxhr. Apparent clearance can be reduced by 56% in patients with hepatic impairment.[label] |
Formulation & handling
- Low aqueous solubility and high lipophilicity may require solubility‑enhancing approaches for oral solid dosage forms.
- Oral administration is not food‑dependent, allowing flexible dosing relative to meals.
- Solid, high‑LogP API may benefit from controlled particle size and protective handling to ensure consistent dissolution performance.
Regulatory status
| Lifecycle | Key U.S. and Canadian patents expired between 2012 and 2017, indicating that the API is now in a mature post‑exclusivity phase. With products marketed in Canada, the US, and the EU, the API is established across major regulated markets. |
|---|
| Markets | Canada, US, EU |
|---|
Supply Chain
| Supply chain summary | Raloxifene’s originator is Eli Lilly, with a broad network of secondary packagers supporting distribution across North America and other regulated markets. Branded products are established in the US, EU, and Canada, indicating mature global availability. Key patents in the US and Canada have expired, suggesting that generic competition is already present or well‑established. |
|---|
Safety
| Toxicity | **LD<sub>50</sub> and Overdose** The oral LD<sub>50</sub> value in rats is > 5000 mg/kg, which is about 810 times the human dose.[MSDS] In monkeys, no mortality was seen after a single oral dose of 1000 mg/kg.[label] No cases of raloxifene overdose have been reported during clinical trials. A rare postmarketing report of a non-fatal overdose after oral ingestion of 1.5 g has been reported. Common adverse events of leg cramps, hot flushes, and dizziness have been reported with the use of raloxifene at doses of greater than 180 mg. More serious adverse event of venous thromboembolic events were observed with raloxifene.Two 18-month-old children accidentally ingested 180 mg of raloxifene and symptoms of ataxia, dizziness, vomiting, rash, diarrhea, tremor, flushing, and elevated alkaline phosphatase levels were reported. There is no known antidote for raloxifene. [label] **Nonclinical Toxicology** In a two-year mouse carcinogenicity study at raloxifene doses that are higher than the human therapeutic doses, there was an increased incidence of benign and malignant ovarian tumors of granulosa or theca cell origin. Another study showed an increased incidence of testicular interstitial cell tumors, prostatic adenomas, adenocarcinomas, and prostatic leiomyoblastoma in male mice receiving doses higher than human therapeutic doses. There was no evidence of the genotoxic potential of raloxifene in bacterial mutagenicity assays, _in vitro_ rat DNA assays, or other _in vitro_ rodent cell line assays. When assessing effects on the reproductive system of male and female rats, raloxifene caused lack of pregnancy and disruptions in estrous cycles and inhibited ovulation at dose of 0.1 to 10 mg/kg/day. Administration of raloxifene during the preimplantation period at doses greater than 0.1 mg/kg resulted in delayed and disrupted embryo implantation, further leading to prolonged gestation and reduced litter size. There were no effects on sperm production or quality or reproductive performance in male rats. The effects on the fertility by raloxifene were reversible.[label] **Use in special populations** The use of raloxifene in pregnant or nursing women is not advised. Although there are no specific dosing adjustment guidelines, caution should be undertaken when administering raloxifene in geriatric patients or patients with renal or hepatic impairment.[label] |
|---|
High Level Warnings:
- High acute oral tolerance in animals (rat LD50 › 5000 mg/kg), but overdose exposures have produced neurologic and gastrointestinal symptoms
- No specific antidote is identified
- Clinically observed adverse effects at elevated doses include leg cramps, hot flushes, dizziness, and rare venous thromboembolic events
Raloxifene is a type of Estrogens
Estrogens are a subcategory of pharmaceutical active pharmaceutical ingredients (APIs) that play a crucial role in hormone therapy and women's health. Estrogens are a class of steroidal compounds that are primarily produced in the ovaries and play a significant role in the development and maintenance of female reproductive tissues and secondary sexual characteristics. These APIs are widely used in various pharmaceutical formulations, including oral contraceptives, hormone replacement therapies, and treatments for menopausal symptoms. They are also utilized in the management of conditions such as hypogonadism, infertility, and certain types of cancer.
Estrogens exert their effects by binding to estrogen receptors, which are present in various tissues throughout the body. This binding initiates a cascade of cellular and molecular events that regulate gene expression and modulate physiological processes.
Some common examples of estrogens used in pharmaceutical formulations include estradiol, estrone, and estriol. These compounds are typically synthesized from natural sources or derived from plant-based substances through a series of chemical reactions and purification processes.
As with any pharmaceutical API, the production of estrogens follows strict quality control guidelines to ensure purity, potency, and safety. Stringent regulatory standards and rigorous testing protocols are employed to guarantee consistent quality and adherence to pharmaceutical industry regulations.
In conclusion, estrogens are a vital subcategory of pharmaceutical APIs with a wide range of applications in women's health and hormone therapy. Their role in maintaining hormonal balance and addressing various medical conditions underscores their importance in modern medicine.
Raloxifene (Estrogens), classified under Hormonal Agents
Hormonal agents are a prominent category of pharmaceutical active pharmaceutical ingredients (APIs) widely used in the medical field. These substances play a crucial role in regulating and modulating hormonal functions within the body. Hormonal agents are designed to mimic or manipulate the effects of naturally occurring hormones, allowing healthcare professionals to treat various endocrine disorders and hormonal imbalances.
Hormonal agents are commonly employed in the treatment of conditions such as hypothyroidism, hyperthyroidism, diabetes, and hormonal cancers. These APIs work by interacting with specific hormone receptors, either by stimulating or inhibiting their activity, to restore the balance of hormones in the body. They can be administered orally, intravenously, or through other routes depending on the specific medication and patient needs.
Pharmaceutical companies employ rigorous manufacturing processes and quality control measures to ensure the purity, potency, and safety of hormonal agent APIs. These APIs are synthesized using chemical or biotechnological methods, often starting from natural hormone sources or through recombinant DNA technology. Stringent regulatory guidelines are in place to guarantee the efficacy and safety of hormonal agent APIs, ensuring that patients receive high-quality medications.
As the demand for hormone-related therapies continues to grow, ongoing research and development efforts focus on enhancing the effectiveness and reducing the side effects of hormonal agent APIs. This includes the exploration of novel delivery systems, advanced formulations, and targeted drug delivery methods. By continuously advancing our understanding and capabilities in hormonal agents, the medical community can improve patient outcomes and quality of life for individuals with hormonal disorders.
Raloxifene API manufacturers & distributors
Compare qualified Raloxifene API suppliers worldwide. We currently have 14 companies offering Raloxifene API, with manufacturing taking place in 4 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Apotex Pharmachem | Producer | India | India | CEP, CoA, GMP, USDMF, WC | 10 products |
| Cambrex | Producer | Italy | Unknown | CoA, JDMF, USDMF | 104 products |
| Cipla | Producer | India | India | CoA, USDMF | 164 products |
| Dr. Reddy's | Producer | India | India | BSE/TSE, CEP, CoA, FDA, GMP, KDMF, MSDS, USDMF, WC | 170 products |
| Erregierre | Producer | Italy | Italy | CEP, CoA, FDA, GMP, JDMF, USDMF | 44 products |
| Global Pharma Tek | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, ISO9001, MSDS | 484 products |
| Glochem | Producer | India | India | CEP, CoA, FDA, GMP, WC | 14 products |
| Hanmi Fine Chemical | Producer | South Korea | South Korea | CoA, JDMF | 18 products |
| Hetero Drugs | Producer | India | Unknown | CEP, CoA, FDA, GMP, USDMF, WC | 98 products |
| Raks Pharma | Producer | India | India | CoA, USDMF | 58 products |
| Sai-Tech Pharmaceuticals ... | Producer | India | India | CoA | 8 products |
| SETV Global | Producer | India | India | CoA, FDA, GMP | 515 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
| Torrent Pharma | Producer | India | India | CoA, USDMF | 34 products |
When sending a request, specify which Raloxifene API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Raloxifene API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
Frequently asked questions about Raloxifene API
Sourcing
What matters most when sourcing GMP-grade Raloxifene?
When sourcing GMP‑grade Raloxifene, ensure the manufacturer complies with GMP requirements recognized in the US, EU, and Canada. Verify that the product comes from a supplier with clear regulatory documentation and an established distribution pathway, as branded and generic products are already mature in these markets. It is also important to confirm traceability through any secondary packaging partners involved in the supply chain.
Which documents are typically required when sourcing Raloxifene API?
Request the core API documentation set: CoA (14 companies), USDMF (8 companies), GMP (8 companies), FDA (7 companies), CEP (5 companies). Confirm versions and validity dates match the destination market to avoid delays in qualification.
Which manufacturers are known to produce Raloxifene API?
Known or reported manufacturers for Raloxifene: Global Pharma Tek, SETV Global, Tenatra Exports Private Limited. Evaluate their GMP history, scale, and regional coverage before requesting dossiers or allocating demand.
How can I request quotes for Raloxifene API from GMP suppliers?
Submit quote requests through the supplier listings with your specs and required documents (specifications, target volume, delivery timeline, and destination). Providing consistent details upfront speeds comparable offers and clarifies technical feasibility.
Is a GMP audit report available for Raloxifene manufacturers?
Audit reports may be requested for Raloxifene: 7 GMP audit reports available. Confirm the scope and recency of any audit before relying on it for qualification decisions.
How many suppliers offer Raloxifene API on Pharmaoffer?
Reported supplier count for Raloxifene: 14 verified suppliers. Filter listings by certifications, regions, and delivery options to match your qualification plan.
Which countries are known to manufacture Raloxifene API?
Production countries reported for Raloxifene: India (10 producers), Italy (1 producer), South Korea (1 producer). Knowing the manufacturing geography helps anticipate logistics lead times and import compliance needs.
Which certifications do suppliers of Raloxifene usually hold?
Common certifications for Raloxifene suppliers: CoA (14 companies), USDMF (8 companies), GMP (8 companies), FDA (7 companies), CEP (5 companies). Always verify issuing authorities and expiry dates when reviewing audit packages.
Technical
What is Raloxifene (CAS 84449-90-1) used for?
Raloxifene is used to prevent and treat osteoporosis in postmenopausal women, including cases related to corticosteroid use. It also reduces the risk of invasive estrogen receptor‑positive breast cancer in postmenopausal women with osteoporosis or those at high risk for breast cancer. Its effects arise from estrogen‑agonist activity in bone and antagonist activity in breast and uterine tissues.
Which therapeutic class does Raloxifene fall into?
Raloxifene belongs to the following therapeutic categories: BCRP/ABCG2 Substrates, Benzene Derivatives, Benzylidene Compounds, Bone Density Conservation Agents, Cytochrome P-450 CYP2B6 Inhibitors. This positioning helps teams compare alternative APIs, anticipate pharmacology expectations, and align early research priorities.
What conditions is Raloxifene mainly prescribed for?
The primary indications for Raloxifene: Indicated for the prevention and treatment of osteoporosis in postmenopausal women, as well as prevention and treatment of corticosteroid-induced bone loss, [label], Indicated for the reduction in the risk of invasive breast cancer in postmenopausal women with osteoporosis or postmenopausal women with a high risk for invasive breast cancer, [label]. These use cases frame the target patient populations and help prioritize formulation and safety evaluations.
How does Raloxifene work?
Raloxifene is a selective estrogen receptor modulator that acts as both an estrogen agonist and antagonist via differential effects on the tissue-specific estrogen receptors. Based on the findings of competitive binding assays, Raloxifene displays binding affinity that is similar to that of [estradiol], the predominant circulating estrogen.Estrogens play variable roles at different tissues in females, including the bone, breasts, uterus and liver, by binding to the steroid nuclear hormone receptors, Estrogen Receptor alpha (ERα) or Estrogen Receptor beta (ERβ).These receptors are normally bound to the Heat Shock Protein 90 (Hsp90) when unbound to the ligand. Ligand binding induces a conformational change in the receptor that promotes dissociation of the receptor from Hsp90, dimerization and translocation into the nucleus. This movement into the nucleus allows the receptor to bind to genomic locations based on sequence recognition of the DNA binding domain, also known as the Estrogen Response Elements (EREs).
In bones, endogenous estrogens normally modulate multiple DNA response elements, including the gene-encoding transforming growth factor-β3 (TGF-β3), which is a cytokine embedded in the bone matrix.TGF-β3 plays an important role in bone remodellingby working with other cytokines to induce production of osteoblasts, such as IL-6, and attenuate the activity of osetoclasts. Estrogens typically maintain the bone integrity by inhibiting the cytokines that recruit osteoclasts and oppose the bone-resorbing, Ca2+-mobilizing action of parathyroid hormone. In contrast, estrogens promote osteoblast proliferation, augment the production of TGF-β3 and bone morphogenic proteins, and inhibit apoptosis.Mimicking the action of endogenous estrogen in bone tissues, Raloxifene binds to the estrogen receptor to influence gene transcription through interactions with the estrogen response element (ERE) and a distinct DNA target, the Raloxifene response element (RRE).It occupies the same ER ligand binding site as estrogen.Upon binding, Raloxifene induces a conformational change of the receptor, allowing mediation of direct binding to transcriptional elements by accessory proteins. Increased expression of bone matrix proteins, such as alkaline phosphatase, osteonectin, osteocalcin and collagen may be seen.The agonistic or antagonistic action of Raloxifene depends on the extent of recruitment of coactivators and corepressors to estrogen receptor (ER) target gene promotors.[label] In breast tissues, Raloxifene acts as an estrogen receptor antagonist to attenuate the estrogen-dependent proliferative effects of epithelial cell expansion. In addition to the antiproliferative effects, Raloxifene prevents the production of cytokines and recruitment of macrophages and lymphocytes into tumor mass.
What should someone know about the safety or toxicity profile of Raloxifene?
Raloxifene shows high acute oral tolerance in animals, but overdose can lead to neurologic and gastrointestinal symptoms, and no specific antidote is available. Common adverse effects at higher exposures include leg cramps, hot flushes, and dizziness. The drug carries a recognized risk of venous thromboembolic events and, in certain high‑risk populations, an increased incidence of fatal stroke. It does not cause endometrial proliferation.
What are important formulation and handling considerations for Raloxifene as an API?
Important considerations include addressing Raloxifene’s low aqueous solubility and high lipophilicity, which may necessitate solubility‑enhancing strategies and controlled particle‑size distribution to achieve consistent dissolution. The API should be handled to protect solid‑state integrity and maintain uniformity during blending and compression. Its lack of food‑dependent absorption supports flexible oral dosing without the need for meal‑related formulation adjustments.
Is Raloxifene a small molecule?
Raloxifene is classified as a small molecule. That classification shapes process design, impurity profiling, and analytical control strategies.
Are there special stability concerns for oral Raloxifene?
Raloxifene’s low aqueous solubility and high lipophilicity require attention to particle‑size control and solubility‑enhancing strategies to maintain consistent dissolution in oral solid forms. The solid, high‑LogP nature of the API may also necessitate protective handling to prevent changes in physical form that could affect performance. These factors, rather than food effects, represent the primary stability considerations for oral formulations.
Regulatory
Where is Raloxifene approved or in use globally?
Raloxifene is reported as approved in the following major regions: Canada, US, EU. Understanding geographic coverage informs regulatory filings, supply planning, and risk assessments before escalating procurement.
What’s the regulatory and patent landscape for Raloxifene right now?
Raloxifene is approved for use in Canada, the United States, and the European Union. It is considered a mature active ingredient, and its original patent protections have expired, allowing broad generic availability in major markets.
Pharmaoffer
How does Pharmaoffer’s Smart Sourcing Service help with Raloxifene procurement?
Pharmaoffer's Smart Sourcing Service coordinates compliant suppliers, documentation, and competitive quotes for Raloxifene. It centralizes outreach, follow-ups, and document validation to shorten procurement timelines.
Is Raloxifene included in the PRO Data Insights coverage?
PRO Data Insights coverage for Raloxifene: 305 verified transactions across 82 suppliers and 53 buyers worldwide. Use the dataset to benchmark suppliers and monitor regulatory activity where available.
Where can I access the API market report for Raloxifene?
Market report availability for Raloxifene: Report Available. The report highlights demand trends, pricing drivers, and supplier landscape insights for procurement planning.
