CERTICAN 0.75MG
EVEROLIMUS
What it does
Everolimus is a medication used to treat certain types of cancer and other serious conditions.
Commonly used for: certain cancers (e.g., breast cancer, kidney cancer), tuberous sclerosis complex, preventing organ transplant rejection
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Source this medicineRegistration & product details
Source: Pharmacy and Poisons Board · fetched 2026-01-28 20:06:02 · updated 2026-09-25 02:11:26
Drug Interactions
53Severe (4)
Everolimus - increases exposure
Grapefruitjuiceispredictedtoincreasetheexposureto everolimus.Avoid.rTheoretical r
Everolimus - decreases exposure
Lumacaftorispredictedtodecreasetheexposureto everolimus.Avoid.rTheoretical
Everolimus - increases exposure
Selpercatinib is predicted to increase the exposure to everolimus. Avoid.
Everolimus - increases exposure
Clarithromycinispredictedtoincreasetheexposureto everolimus.Avoid.rStudy https://www.facebook.c (Books-Courses-Medic
Moderate (26)
Everolimus - increases concentration
Dronedarone is predicted to increase the concentration of everolimus. Avoid or adjust dose.
Everolimus - increases concentration
Antifungals, azoles (fluconazole, isavuconazole, posaconazole) are predicted to increase the concentration of everolimus. Avoid or adjust dose.
Everolimus - decreases exposure
Belzutifanispredictedtodecreasetheexposuretoeverolimus. Avoidoradjustdose.rTheoretical
Everolimus - increases concentration
Berotralstat is predicted to increase the concentration of everolimus. Monitor and adjust dose.
Everolimus - increases exposure
Cannabidiol moderately increases the exposure to everolimus. Monitor and adjust dose.
Unknown (23)
Everolimus - increases exposure
Abrocitinibmightincreasetheexposuretoeverolimus. oTheoretical
Everolimus - increases exposure
Asciminibispredictedtoincreasetheexposuretoeverolimus. rTheoretical
Everolimus - increases exposure
Bulevirtideispredictedtoincreasetheexposuretoeverolimus. oTheoretical
Everolimus - increases exposure
Ceritinibispredictedtoincreasetheexposuretoeverolimus. oTheoretical
Everolimus - increases exposure
Cobicistat is predicted to increase the exposure to everolimus. Avoid.
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About this medicine
Everolimus is a medication used to treat certain types of cancer and other serious conditions.
What it treats
- certain cancers (e.g., breast cancer, kidney cancer)
- tuberous sclerosis complex
- preventing organ transplant rejection
How it works
Everolimus works by stopping the growth of cancer cells and suppressing the immune system to prevent organ rejection.
Who it's for
This medication is for adults and, in some cases, children with specific medical conditions.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Everolimus
BNF-referencedEverolimus is a potent mTOR (mechanistic Target of Rapamycin) inhibitor, primarily used in oncology for the treatment of various malignancies, particularly those responsive to targeted therapies. It is administered orally and has applications in managing neuroendocrine tumors, renal cell carcinoma, and as an adjunct therapy for certain types of seizures associated with tuberous sclerosis complex. Everolimus's mechanism of action involves inhibiting cell growth and proliferation by blocking signal transduction pathways critical for tumor growth.
Indications
- Neuroendocrine tumors of pancreatic origin
- Neuroendocrine tumors of gastrointestinal origin
- Renal cell carcinoma
- Subependymal giant cell astrocytoma associated with tuberous sclerosis complex
- Adjunctive treatment of refractory partial-onset seizures associated with tuberous sclerosis complex
Dosage
Adults: Initially 10 mg once daily, adjusted based on response and tolerability. For renal transplantation, start approximately 4 weeks post-transplantation at an initial dose of 1 mg twice daily.
Mechanism of action
Everolimus binds with high affinity to FK506 binding protein-12 (FKBP-12), forming a complex that inhibits mTOR activation. This inhibition leads to reduced activity of downstream effectors, causing cell cycle arrest in the G1 phase, and ultimately triggering apoptosis. Additionally, everolimus suppresses the expression of hypoxia-inducible factor, decreasing vascular endothelial growth factor levels, which results in reduced cell proliferation and angiogenesis.
Pharmacodynamics
Everolimus exhibits its pharmacological effects by impeding cellular processes involved in growth and metabolism. It effectively reduces the proliferation of cancer cells by inhibiting mTORC1, which is pivotal in protein synthesis and cell growth regulation. Its anti-angiogenic properties stem from the reduction of vascular endothelial growth factor, further curtailing tumor growth and metastasis.
Pharmacokinetics
Everolimus is orally bioavailable, with peak plasma concentrations occurring approximately 1 to 2 hours after administration. It is extensively metabolized by the liver, primarily via CYP3A4, with a half-life of about 30 hours. The drug's pharmacokinetics can be significantly affected by food, hepatic function, and drug interactions, particularly with strong CYP3A4 inhibitors or inducers.
Contra-indications
- Severe liver impairment
- History of bleeding disorders peri-surgical period
Adverse effects
- Alopecia
- Anaemia
- Appetite changes
- Increased risk of infections
- Mouth ulcers
- Nausea
- Fatigue
- Diarrhea
Interactions
- Grapefruit juice increases exposure
- Lumacaftor decreases exposure
- Selpercatinib increases exposure
- Clarithromycin increases exposure
- Dronedarone increases concentration
- Antifungals (azoles) increase concentration
- Belzutifan decreases exposure
- Berotralstat increases concentration
- Cannabidiol increases exposure
- Cenobamate decreases exposure
Precautions
- Monitor liver function regularly
- Adjust dose based on renal function
- Consider monitoring for signs of infection due to immunosuppression
Pregnancy
Limited data on the use of everolimus in pregnancy. Potential risks should be weighed against the benefits. Consult relevant guidelines.
Breast-feeding
Lactation studies are limited. Caution is advised when administering to nursing mothers.
Storage
Store at room temperature, away from moisture and heat. Keep out of reach of children.
Formulations
- Tablets (Certican®)
- Dispersible tablets (Votubia®)
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Everolimus
PubChem CID 6442177Molecular formula: C53H83NO14
Mechanism of action
Everolimus is a mTOR inhibitor that binds with high affinity to the FK506 binding protein-12 (FKBP-12), thereby forming a drug complex that inhibits the activation of mTOR. This inhibition reduces the activity of effectors downstream, which leads to a blockage in the progression of cells from G1 into S phase, and subsequently inducing cell growth arrest and apoptosis. Everolimus also inhibits the expression of hypoxia-inducible factor, leading to a decrease in the expression of vascular endothelial growth factor. The result of everolimus inhibition of mTOR is a reduction in cell proliferation, angiogenesis, and glucose uptake. Mechanistic target of rapamycin (mTOR) is a serine-threonine kinase that functions via two multiprotein complexes, namely mTORC1 and mTORC2, each characterized by different binding partners that confer separate functions. mTORC1 function is tightly regulated by PI3-K/Akt and is sensitive to rapamycin. mTORC2 is sensitive to growth factors, not nutrients, and is associated with rapamycin-insensitivity. mTORC1 regulates protein synthesis and cell growth through downstream molecules: 4E-BP1 (also called EIF4E-BP1) and S6K. Also, mTORC2 is thought to modulate growth factor signaling by phosphorylating the C-terminal hydrophobic motif of some AGC kinases such as Akt and SGK. Recent evidence has suggested that mTORC2 may play an important role in maintenance of normal as well as cancer cells by virtue of its association with ribosomes, which may be involved in metabolic regulation of the cell. Rapamycin (sirolimus) and its analogs known as rapalogues, such as RAD001 (everolimus) and CCI-779 (temsirolimus), suppress mTOR activity through an allosteric mechanism that acts at a distance from the ATP-catalytic binding site, and are considered incomplete inhibitors. Moreover, these compounds suppress mTORC1-mediated S6K activation, thereby blocking a negative feedback loop, leading to activation of mitogenic pathways promoting cell survival and growth. Consequently, mTOR is a suitable target of therapy in cancer treatments. However, neither of these complexes is fully inhibited by the allosteric inhibitor rapamycin or its analogs. In recent years, new pharmacologic agents have been developed which can inhibit these complexes via ATP-binding mechanism, or dual inhibition of the canonical PI3-K/Akt/mTOR signaling pathway. These compounds include WYE-354, KU-003679, PI-103, Torin1, and Torin2, which can target both complexes or serve as a dual inhibitor for PI3-K/mTOR. This investigation describes the mechanism of action of pharmacological agents that effectively target mTORC1 and mTORC2 resulting in suppression of growth, proliferation, and migration of tumor and cancer stem cells. Mammalian target of rapamycin (mTOR) inhibitors have anti-tumor effects against renal cell carcinoma, pancreatic neuroendocrine cancer and breast cancer. In this study, we analyzed the antitumor effects of mTOR inhibitors in small cell lung cancer (SCLC) cells and sought to clarify the mechanism of resistance to mTOR inhibitors. We analyzed the antitumor effects of three mTOR inhibitors including everolimus in 7 SCLC cell lines by MTS assay. Gene-chip analysis, receptor tyrosine kinases (RTK) array and Western blotting analysis were performed to identify molecules associated with resistance to everolimus. Only SBC5 cells showed sensitivity to everolimus by MTS assay. We established two everolimus resistant-SBC5 cell lines (SBC5 R1 and SBC5 R10) by continuous exposure to increasing concentrations of everolimus stepwise. SPP1 and MYC were overexpressed in both SBC5 R1 and SBC5 R10 by gene-chip analysis. High expression levels of eukaryotic translation initiation factor 4E (eIF4E) were observed in 5 everolimus-resistant SCLC cells and SBC5 R10 cells by Western blotting. MYC siRNA reduced eIF4E phosphorylation in SBC5 cells, suggesting that MYC directly activates eIF4E by an mTOR-independent bypass pathway. Importantly, after reduction of MYC
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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The same active ingredient registered across other registries we cover - including different brands.