Lenalidomide 2.5mg capsules
Prescription only
Requires a prescription from a doctor or prescriber
Capsule
2.5mg
Oral
Drugs affecting the immune response
Active ingredients:
Lenalidomide
1 safety notice
Safety information for pregnancy and breastfeeding
Pregnancy
Toxicities associated with lenalidomide, some leading to fatality, include embryo-fetal toxicity, neutropenia, thrombocytopenia, venous (deep vein thrombosis and pulmonary embolism) and arterial thromboembolic events (myocardial infarction and stroke), serious adverse cardiovascular reactions, second primary malignancies, hepatotoxicity, severe cutaneous reactions, tumour lysis syndrome, tumour flare reaction, hypothyroidism, and hyperthyroidism.[L16028]
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Lenalidomide
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Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
EMA
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Lenalidomide
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
12 branded products available
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12 products
MHRA licensed products
View all licensed products for Lenalidomide on the MHRA register
Revlimid 2.5mg capsules
Lenalidomide 2.5mg capsules
Lenalidomide 2.5mg capsules
Lenalidomide 2.5mg capsules
Lenalidomide 2.5mg capsules
Lenalidomide 2.5mg capsules
Lenalidomide 2.5mg capsules
Lenalidomide 2.5mg capsules
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WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Lenalidomide
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(11)
Carfilzomib with dexamethasone and lenalidomide for previously treated multiple myeloma (TA695)
TA695
Technology appraisal
Updated Apr 2021Lenalidomide plus dexamethasone for previously untreated multiple myeloma (TA587)
TA587
Technology appraisal
Updated Jun 2019Lenalidomide with rituximab for previously treated follicular lymphoma (TA627)
TA627
Technology appraisal
Updated Apr 2020Lenalidomide plus dexamethasone for multiple myeloma after 1 treatment with bortezomib (TA586)
TA586
Technology appraisal
Updated Jun 2019Lenalidomide for treating myelodysplastic syndromes associated with an isolated deletion 5q cytogenetic abnormality (TA322)
TA322
Technology appraisal
Updated Jun 2019Daratumumab with lenalidomide and dexamethasone for untreated multiple myeloma when a stem cell transplant is unsuitable (TA917)
TA917
Technology appraisal
Updated Oct 2023Ixazomib with lenalidomide and dexamethasone for treating relapsed or refractory multiple myeloma (TA870)
TA870
Technology appraisal
Updated Feb 2023Tafasitamab with lenalidomide for treating relapsed or refractory diffuse large B-cell lymphoma (TA883)
TA883
Technology appraisal
Updated May 2023Lenalidomide maintenance treatment after an autologous stem cell transplant for newly diagnosed multiple myeloma (TA680)
TA680
Technology appraisal
Updated Mar 2021Lenalidomide for the treatment of multiple myeloma in people who have received at least 2 prior therapies (TA171)
TA171
Technology appraisal
Updated Jun 2019Pomalidomide for multiple myeloma previously treated with lenalidomide and bortezomib (TA427)
TA427
Technology appraisal
Updated Jan 2017Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
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These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Lenalidomide is a drug with multiple mechanisms of action.
Food interactions
2 warnings
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
77 ng/ml
Following oral administration, lenalidomide is rapidly absorbed with high bioavailability.
[A228628]…
[A228628]…
Half-life
5–50 mg
In healthy subjects, the mean half-life of lenalidomide is three hours in the clinically relevant dose range (5–50 mg).
[A228628]…
[A228628]…
Protein binding
30%
In vitro, about 30% of lenalidomide was bound to plasma proteins.
[L16028]
[L16028]
Volume of distribution
7.3 L
In healthy male subjects, the apparent volume of distribution was 75.8 ± 7.3 L.
[A228628]
[A228628]
Metabolism
Lenalidomide is not subject to extensive hepatic metabolism involving CYP enzymes and metabolism contributes to a very minor extent to the clearance of lenalidomide in humans.…
Elimination
25 mg
Lenalidomide is eliminated predominantly via urinary excretion in the unchanged form.…
Clearance
41 mL/min
The renal clearance of lenalidomide exceeds the glomerular filtration rate.
[L16028]…
[L16028]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Lenalidomide (previously referred to as CC-5013) is an immunomodulatory drug with potent antineoplastic, anti-angiogenic, and anti-inflammatory properties.[A228553] It is a 4-amino-glutamyl analogue of [thalidomide] [A228543] and like thalidomide, lenalidomide exists as a racemic mixture of the active S(-) and R(+) forms.[A228708] However, lenalidomide is much safer and potent than thalidomide, with fewer adverse effects and toxicities.[A714][A228543] Thalidomide and its analogues, including lenalidomide, are referred to as immunomodulatory imide drugs (also known as cereblon modulators), which are a class of immunomodulatory drugs that contain an imide group. Lenalidomide works through various mechanisms of actions that promote malignant cell death and enhance host immunity.[A228708] Available as oral capsules, lenalidomide is approved by the FDA and EU for the treatment of multiple myeloma, myelodysplastic syndromes, mantle cell lymphoma, follicular lymphoma, and marginal zone lymphoma in selected patients.[L16028] Due to severe teratogenicity, pregnancy must be excluded before the start of treatment and patients must enroll in the lenalidomide Risk Evaluation and Mitigation Strategy (REMS) program to ensure contraception adherence.[A228708]
Properties:
View FDA drug labelsolid
Avg. mass: 259.26 Da
DrugBank indication
Lenalidomide is indicated for the treatment of adult patients with multiple myeloma (MM) in combination with dexamethasone. It is also indicated as maintenance therapy in multiple myeloma following autologous hematopoietic stem cell transplantation (auto-HSCT).
It is indicated for the treatment of adult patients with transfusion-dependent anemia due to low- or intermediate-1-risk myelodysplastic syndromes (MDS) associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities.
Lenalidomide is indicated for the treatment of adult patients with mantle cell lymphoma (MCL) whose disease has relapsed or progressed after two prior therapies, one of which included bortezomib.
In combination with a rituximab product, lenalidomide is indicated for the treatment of adult patients with previously treated follicular lymphoma (FL) or previously treated marginal zone lymphoma (MZL).
[L16028]
It is indicated for the treatment of adult patients with transfusion-dependent anemia due to low- or intermediate-1-risk myelodysplastic syndromes (MDS) associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities.
Lenalidomide is indicated for the treatment of adult patients with mantle cell lymphoma (MCL) whose disease has relapsed or progressed after two prior therapies, one of which included bortezomib.
In combination with a rituximab product, lenalidomide is indicated for the treatment of adult patients with previously treated follicular lymphoma (FL) or previously treated marginal zone lymphoma (MZL).
[L16028]
Also known as(37)
1-oxo-2-(2,6-dioxopiperidin-3-yl)-4-aminoisoindoline
3-(4-Amino-1-oxoisoindolin-2-yl)piperidine-2,6-dione
Lena
Lenalidomida
Lenalidomide
ODF
OPGL
Osteoclast differentiation factor
Dosage forms(33)
Capsule (Oral) — 5.000 mg
Capsule (Oral) — 2.5 MG
Capsule (Oral)
Capsule, coated (Oral) — 15 mg
Capsule, coated (Oral) — 25 mg
Capsule, coated (Oral) — 5 mg
Capsule (Oral) — 15.000 mg
Capsule, coated (Oral) — 20 mg
Molecular properties(17)
Drug interactions(1207)
Known interactions with other medications. Always consult a healthcare professional.
The risk or severity of adverse effects can be increased when Denosumab is combined with Lenalidomide.
Etanercept
Unknown severity
The risk or severity of adverse effects can be increased when Etanercept is combined with Lenalidomide.
Peginterferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2a is combined with Lenalidomide.
Interferon alfa-n1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n1 is combined with Lenalidomide.
Interferon alfa-n3
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n3 is combined with Lenalidomide.
Peginterferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2b is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Anakinra is combined with Lenalidomide.
Interferon gamma-1b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon gamma-1b is combined with Lenalidomide.
Interferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-2a is combined with Lenalidomide.
Aldesleukin
Unknown severity
The risk or severity of adverse effects can be increased when Aldesleukin is combined with Lenalidomide.
Adalimumab
Unknown severity
The risk or severity of adverse effects can be increased when Adalimumab is combined with Lenalidomide.
Gemtuzumab ozogamicin
Unknown severity
The risk or severity of adverse effects can be increased when Gemtuzumab ozogamicin is combined with Lenalidomide.
Pegaspargase
Unknown severity
The risk or severity of adverse effects can be increased when Pegaspargase is combined with Lenalidomide.
Infliximab
Unknown severity
The risk or severity of adverse effects can be increased when Infliximab is combined with Lenalidomide.
Interferon beta-1b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon beta-1b is combined with Lenalidomide.
Interferon alfacon-1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfacon-1 is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Rituximab is combined with Lenalidomide.
Basiliximab
Unknown severity
The risk or severity of adverse effects can be increased when Basiliximab is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Muromonab is combined with Lenalidomide.
Ibritumomab tiuxetan
Unknown severity
The risk or severity of adverse effects can be increased when Ibritumomab tiuxetan is combined with Lenalidomide.
Tositumomab
Unknown severity
The risk or severity of adverse effects can be increased when Tositumomab is combined with Lenalidomide.
Alemtuzumab
Unknown severity
The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Alefacept is combined with Lenalidomide.
Efalizumab
Unknown severity
The risk or severity of adverse effects can be increased when Efalizumab is combined with Lenalidomide.
Antithymocyte immunoglobulin (rabbit)
Unknown severity
The risk or severity of adverse effects can be increased when Antithymocyte immunoglobulin (rabbit) is combined with Lenalidomide.
Interferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-2b is combined with Lenalidomide.
Daclizumab
Unknown severity
The risk or severity of adverse effects can be increased when Daclizumab is combined with Lenalidomide.
Phenylalanine
Unknown severity
The risk or severity of adverse effects can be increased when Phenylalanine is combined with Lenalidomide.
Flunisolide
Unknown severity
The risk or severity of adverse effects can be increased when Flunisolide is combined with Lenalidomide.
Bortezomib
Unknown severity
The risk or severity of adverse effects can be increased when Bortezomib is combined with Lenalidomide.
Cladribine
Moderate
Lenalidomide may increase the immunosuppressive activities of Cladribine.
Carmustine
Unknown severity
The risk or severity of adverse effects can be increased when Carmustine is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Amsacrine is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Bleomycin is combined with Lenalidomide.
Chlorambucil
Unknown severity
The risk or severity of adverse effects can be increased when Chlorambucil is combined with Lenalidomide.
Raltitrexed
Unknown severity
The risk or severity of adverse effects can be increased when Raltitrexed is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Mitomycin is combined with Lenalidomide.
Bexarotene
Unknown severity
The risk or severity of adverse effects can be increased when Bexarotene is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Vindesine is combined with Lenalidomide.
Floxuridine
Unknown severity
The risk or severity of adverse effects can be increased when Floxuridine is combined with Lenalidomide.
Indomethacin
Unknown severity
The risk or severity of adverse effects can be increased when Indomethacin is combined with Lenalidomide.
Tioguanine
Unknown severity
The risk or severity of adverse effects can be increased when Tioguanine is combined with Lenalidomide.
Vinorelbine
Unknown severity
The risk or severity of adverse effects can be increased when Vinorelbine is combined with Lenalidomide.
Dexrazoxane
Unknown severity
The risk or severity of adverse effects can be increased when Dexrazoxane is combined with Lenalidomide.
Beclomethasone dipropionate
Unknown severity
The risk or severity of adverse effects can be increased when Beclomethasone dipropionate is combined with Lenalidomide.
The risk or severity of adverse effects can be increased when Sorafenib is combined with Lenalidomide.
Streptozocin
Unknown severity
The risk or severity of adverse effects can be increased when Streptozocin is combined with Lenalidomide.
Trifluridine
Unknown severity
The risk or severity of adverse effects can be increased when Trifluridine is combined with Lenalidomide.
Gemcitabine
Unknown severity
The risk or severity of adverse effects can be increased when Gemcitabine is combined with Lenalidomide.
Betamethasone
Unknown severity
The risk or severity of adverse effects can be increased when Betamethasone is combined with Lenalidomide.
Showing 50 of 1207 interactions
Food & lifestyle interactions
Advice
Take at the same time every day. Skip the missed dose if it has been more than 12 hours since your regular time.
Advice
Take with or without food. High-fat meals decrease absorption, but not to a clinically significant extent.
Toxicity & overdose
The lowest lethal dose (LDLo) in rats is >2000 mg/kg following oral administration and >40 mg/kg following intravenous administration.
[L31613]
The oral Lowest published toxic dose (TDLo) in humans is 9 mg/kg/4W (intermittent).
[L31623]
There is limited clinical experience in managing lenalidomide overdose. In single-dose studies, healthy subjects have been exposed to doses up to 400 mg. In clinical trials, the dose-limiting toxicity was neutropenia and thrombocytopenia.
Toxicities associated with lenalidomide, some leading to fatality, include embryo-fetal toxicity, neutropenia, thrombocytopenia, venous (deep vein thrombosis and pulmonary embolism) and arterial thromboembolic events (myocardial infarction and stroke), serious adverse cardiovascular reactions, second primary malignancies, hepatotoxicity, severe cutaneous reactions, tumour lysis syndrome, tumour flare reaction, hypothyroidism, and hyperthyroidism.
[L16028]
[L31613]
The oral Lowest published toxic dose (TDLo) in humans is 9 mg/kg/4W (intermittent).
[L31623]
There is limited clinical experience in managing lenalidomide overdose. In single-dose studies, healthy subjects have been exposed to doses up to 400 mg. In clinical trials, the dose-limiting toxicity was neutropenia and thrombocytopenia.
Toxicities associated with lenalidomide, some leading to fatality, include embryo-fetal toxicity, neutropenia, thrombocytopenia, venous (deep vein thrombosis and pulmonary embolism) and arterial thromboembolic events (myocardial infarction and stroke), serious adverse cardiovascular reactions, second primary malignancies, hepatotoxicity, severe cutaneous reactions, tumour lysis syndrome, tumour flare reaction, hypothyroidism, and hyperthyroidism.
[L16028]
How it works
Mechanism of action
Lenalidomide is a drug with multiple mechanisms of action. Lenalidomide exerts immunomodulating effects by altering cytokine production, regulating T cell co-stimulation, and enhancing the NK cell-mediated cytotoxicity.[A228543] Lenalidomide directly inhibits the cullin ring E3 ubiquitin ligase complex: upon binding to cereblon, a substrate adaptor of the complex, lenalidomide modulates substrate specificity of the complex to recruit substrate proteins of the ligase, including Ikaros (IKZF1), Aiolos (IKZF3), and CK1α.[L16028] These substrates are then tagged for ubiquitination and subsequent proteasomal degradation. IKZF1 and IKZF3 are B-cell transcription factors that are essential for B-cell differentiation and survival of malignant cells. IKZF3 also regulates the expression of interferon regulatory factor 4 (IRF4), which is a transcription factor that regulates the aberrant myeloma-specific gene. The immunomodulatory actions of lenalidomide can be partly explained by the degradation of IKZF3, since it is a repressor of the interleukin 2 gene (IL2): as lenalidomide decreases the level of IKZF3, the production of IL-2 increases, thereby increasing the proliferation of natural killer (NK), NKT cells, and CD4+ T cells.[A228703] Lenalidomide inhibits the production of pro-inflammatory cytokines TNF-α, IL-1, IL-6, and IL-12, while elevating the production of anti-inflammatory cytokine IL-10.[A228543] Lenalidomide acts as a T-cell co-stimulatory molecule that promotes CD3 T-cell proliferation and increases the production of IL-2 and IFN-γ in T lymphocytes, which enhances NK cell cytotoxicity and ADCC. It inhibits the expression and function of T-regulatory cells, which are often overabundant in some hematological malignancies.[A228708]
Lenalidomide directly exerts antitumour effects by inhibiting the proliferation and inducing apoptosis of tumour cells. Lenalidomide triggers the activation of pro-apoptotic caspase-8, enhances tumour cell sensitivity to FAS-induced apoptosis, and downregulates NF-κB, an anti-apoptotic protein.[A228708] Independent of its immunomodulatory effects, lenalidomide mediates anti-angiogenic effects by inhibiting angiogenic growth factors released by tumour cells, such as vascular endothelial growth factor (VEGF), basic fibroblastic-growth factor (BFGF), and hepatocyte-growth factor. In vitro, lenalidomide inhibits cell adhesion molecules such as ICAM-1, LFA-1, β2 and β3 integrins, as well as gap-junction function, thereby preventing metastasis of malignant cells.[A228708]
Lenalidomide directly exerts antitumour effects by inhibiting the proliferation and inducing apoptosis of tumour cells. Lenalidomide triggers the activation of pro-apoptotic caspase-8, enhances tumour cell sensitivity to FAS-induced apoptosis, and downregulates NF-κB, an anti-apoptotic protein.[A228708] Independent of its immunomodulatory effects, lenalidomide mediates anti-angiogenic effects by inhibiting angiogenic growth factors released by tumour cells, such as vascular endothelial growth factor (VEGF), basic fibroblastic-growth factor (BFGF), and hepatocyte-growth factor. In vitro, lenalidomide inhibits cell adhesion molecules such as ICAM-1, LFA-1, β2 and β3 integrins, as well as gap-junction function, thereby preventing metastasis of malignant cells.[A228708]
Pharmacodynamics
In hematological malignancies, the immune system is deregulated in the form of altered cytokine networks in the tumour microenvironment, defective T cell regulation of host-tumour immune interactions, and diminished NK cell activity.[A228543] Lenalidomide is an immunomodulatory agent with antineoplastic, antiangiogenic, and anti-inflammatory properties.[A228628] Lenalidomide exerts direct cytotoxicity by increasing apoptosis and inhibiting the proliferation of hematopoietic malignant cells.[A228708] It delays tumour growth in nonclinical hematopoietic tumour models in vivo, including multiple myeloma.[L16028] Lenalidomide also works to limit the invasion or metastasis of tumour cells and inhibits angiogenesis.[A228708]
Lenalidomide also mediates indirect antitumour effects via its immunomodulatory actions: it inhibits the production of pro-inflammatory cytokines, which are implicated in various hematologic malignancies. Lenalidomide enhances the host immunity by stimulating T cell proliferation and enhancing the activity of natural killer (NK) cells.[A713][A228703][A228708] Lenalidomide is about 100–1000 times more potent in stimulating T cell proliferation than [thalidomide].[A228543] In vitro, it enhances antibody-dependent cell-mediated cytotoxicity (ADCC), which is even more pronounced when used in combination with rituximab.[L16028] Due to its anti-inflammatory properties, lenalidomide has been investigated in the context of inflammatory and autoimmune diseases, such as amyotrophic lateral sclerosis.[A229418]
Lenalidomide also mediates indirect antitumour effects via its immunomodulatory actions: it inhibits the production of pro-inflammatory cytokines, which are implicated in various hematologic malignancies. Lenalidomide enhances the host immunity by stimulating T cell proliferation and enhancing the activity of natural killer (NK) cells.[A713][A228703][A228708] Lenalidomide is about 100–1000 times more potent in stimulating T cell proliferation than [thalidomide].[A228543] In vitro, it enhances antibody-dependent cell-mediated cytotoxicity (ADCC), which is even more pronounced when used in combination with rituximab.[L16028] Due to its anti-inflammatory properties, lenalidomide has been investigated in the context of inflammatory and autoimmune diseases, such as amyotrophic lateral sclerosis.[A229418]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Following oral administration, lenalidomide is rapidly absorbed with high bioavailability.
[A228628]
It has a Tmax ranging from 0.5 to six hours. Lenalidomide exhibits a linear pharmacokinetic profile, with its AUC and Cmax increasing proportionally with dose. Multiple dosing does not result in drug accumulation.
[L16028]
In healthy male subjects, the Cmax was 413 ± 77 ng/ml and the AUCinfinity was 1319 ± 162 h x ng/ml.
[A228628]
[A228628]
It has a Tmax ranging from 0.5 to six hours. Lenalidomide exhibits a linear pharmacokinetic profile, with its AUC and Cmax increasing proportionally with dose. Multiple dosing does not result in drug accumulation.
[L16028]
In healthy male subjects, the Cmax was 413 ± 77 ng/ml and the AUCinfinity was 1319 ± 162 h x ng/ml.
[A228628]
Half-life
In healthy subjects, the mean half-life of lenalidomide is three hours in the clinically relevant dose range (5–50 mg).
[A228628]
Half-life can range from three to five hours in patients with multiple myeloma, myelodysplastic syndromes, or mantle cell lymphoma.
[L16028]
[A228628]
Half-life can range from three to five hours in patients with multiple myeloma, myelodysplastic syndromes, or mantle cell lymphoma.
[L16028]
Protein binding
In vitro, about 30% of lenalidomide was bound to plasma proteins.
[L16028]
[L16028]
Volume of distribution
In healthy male subjects, the apparent volume of distribution was 75.8 ± 7.3 L.
[A228628]
[A228628]
Metabolism
Lenalidomide is not subject to extensive hepatic metabolism involving CYP enzymes and metabolism contributes to a very minor extent to the clearance of lenalidomide in humans. Lenalidomide undergoes hydrolysis in human plasma to form 5-hydroxy-lenalidomide and N-acetyl-lenalidomide.
[A228628]
Unchanged lenalidomide is the predominant circulating drug form, with metabolites accounting for less than five percent of the parent drug levels in the circulation.
[L16028]
[A228628]
Unchanged lenalidomide is the predominant circulating drug form, with metabolites accounting for less than five percent of the parent drug levels in the circulation.
[L16028]
Route of elimination
Lenalidomide is eliminated predominantly via urinary excretion in the unchanged form. Following oral administration of 25 mg of radiolabeled lenalidomide in healthy subjects, about 90% of the dose (4.59% as metabolites) was eliminated in urine and 4% of the dose (1.83% as metabolites) was eliminated in feces within ten days post-dose. Approximately 85% of the dose was excreted as lenalidomide in the urine within 24 hours.
[L16028]
[L16028]
Clearance
The renal clearance of lenalidomide exceeds the glomerular filtration rate.
[L16028]
In healthy male subjects, the oral clearance was 318 ± 41 mL/min.
[A228628]
[L16028]
In healthy male subjects, the oral clearance was 318 ± 41 mL/min.
[A228628]
Drug targets(5)
Proteins and enzymes this drug interacts with in the body
Protein cereblon
CRBN
inhibitor
Specific functionmetal ion binding
Cellular location
Cytoplasm
General function & pharmacology
Substrate recognition component of a DCX (DDB1-CUL4-X-box) E3 protein ligase complex that mediates the ubiquitination and subsequent proteasomal degradation of target proteins, such as MEIS2, ILF2 or GLUL .
PMID:26990986 PMID:33009960
Normal degradation of key regulatory proteins is required for normal limb outgrowth and expression of the fibroblast growth factor FGF8 .
PMID:20223979 PMID:24328678 PMID:25043012 PMID:25108355
Maintains presynaptic glutamate release and consequently cognitive functions, such as memory and learning, by negatively regulating large-conductance calcium-activated potassium (BK) channels in excitatory neurons .
PMID:18414909 PMID:29530986
Likely to function by regulating the assembly and neuronal surface expression of BK channels via its interaction with KCNT1 .
PMID:18414909
May also be involved in regulating anxiety-like behaviors via a BK channel-independent mechanism (By similarity). Plays a negative role in TLR4 signaling by interacting with TRAF6 and ECSIT, leading to inhibition of ECSIT ubiquitination, an important step of the signaling PMID:31620128
PMID:26990986 PMID:33009960
Normal degradation of key regulatory proteins is required for normal limb outgrowth and expression of the fibroblast growth factor FGF8 .
PMID:20223979 PMID:24328678 PMID:25043012 PMID:25108355
Maintains presynaptic glutamate release and consequently cognitive functions, such as memory and learning, by negatively regulating large-conductance calcium-activated potassium (BK) channels in excitatory neurons .
PMID:18414909 PMID:29530986
Likely to function by regulating the assembly and neuronal surface expression of BK channels via its interaction with KCNT1 .
PMID:18414909
May also be involved in regulating anxiety-like behaviors via a BK channel-independent mechanism (By similarity). Plays a negative role in TLR4 signaling by interacting with TRAF6 and ECSIT, leading to inhibition of ECSIT ubiquitination, an important step of the signaling PMID:31620128
Tumor necrosis factor ligand superfamily member 11
TNFSF11
inhibitor
Specific functioncytokine activity
Cellular location
Cell membrane
General function & pharmacology
Cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. Osteoclast differentiation and activation factor. Augments the ability of dendritic cells to stimulate naive T-cell proliferation.
May be an important regulator of interactions between T-cells and dendritic cells and may play a role in the regulation of the T-cell-dependent immune response. May also play an important role in enhanced bone-resorption in humoral hypercalcemia of malignancy .
PMID:22664871
Induces osteoclastogenesis by activating multiple signaling pathways in osteoclast precursor cells, chief among which is induction of long lasting oscillations in the intracellular concentration of Ca (2+) resulting in the activation of NFATC1, which translocates to the nucleus and induces osteoclast-specific gene transcription to allow differentiation of osteoclasts. During osteoclast differentiation, in a TMEM64 and ATP2A2-dependent manner induces activation of CREB1 and mitochondrial ROS generation necessary for proper osteoclast generation (By similarity)
May be an important regulator of interactions between T-cells and dendritic cells and may play a role in the regulation of the T-cell-dependent immune response. May also play an important role in enhanced bone-resorption in humoral hypercalcemia of malignancy .
PMID:22664871
Induces osteoclastogenesis by activating multiple signaling pathways in osteoclast precursor cells, chief among which is induction of long lasting oscillations in the intracellular concentration of Ca (2+) resulting in the activation of NFATC1, which translocates to the nucleus and induces osteoclast-specific gene transcription to allow differentiation of osteoclasts. During osteoclast differentiation, in a TMEM64 and ATP2A2-dependent manner induces activation of CREB1 and mitochondrial ROS generation necessary for proper osteoclast generation (By similarity)
Tumor necrosis factor
TNF
inhibitor
Specific functioncytokine activity
Cellular location
Cell membrane
General function & pharmacology
Cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation.
Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Up-regulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective .
PMID:23396208
Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line .
PMID:16829952 PMID:22517918 PMID:23396208
Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity).
Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 .
PMID:12794819
Promotes osteoclastogenesis and therefore mediates bone resorption (By similarity)
Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Up-regulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective .
PMID:23396208
Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line .
PMID:16829952 PMID:22517918 PMID:23396208
Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity).
Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 .
PMID:12794819
Promotes osteoclastogenesis and therefore mediates bone resorption (By similarity)
Cadherin-5
CDH5
antagonist
Specific functionbeta-catenin binding
Cellular location
Cell junction, adherens junction
General function & pharmacology
Cadherins are calcium-dependent cell adhesion proteins (By similarity). They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types .
PMID:21269602
This cadherin may play a important role in endothelial cell biology through control of the cohesion and organization of the intercellular junctions (By similarity). It associates with alpha-catenin forming a link to the cytoskeleton .
PMID:10861224
Plays a role in coupling actin fibers to cell junctions in endothelial cells, via acting as a cell junctional complex anchor for AMOTL2 and MAGI1 (By similarity).
Acts in concert with KRIT1 and PALS1 to establish and maintain correct endothelial cell polarity and vascular lumen (By similarity). These effects are mediated by recruitment and activation of the Par polarity complex and RAP1B .
PMID:20332120
Required for activation of PRKCZ and for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction .
PMID:20332120
Associates with CTNND1/p120-catenin to control CADH5 endocytosis (By similarity)
PMID:21269602
This cadherin may play a important role in endothelial cell biology through control of the cohesion and organization of the intercellular junctions (By similarity). It associates with alpha-catenin forming a link to the cytoskeleton .
PMID:10861224
Plays a role in coupling actin fibers to cell junctions in endothelial cells, via acting as a cell junctional complex anchor for AMOTL2 and MAGI1 (By similarity).
Acts in concert with KRIT1 and PALS1 to establish and maintain correct endothelial cell polarity and vascular lumen (By similarity). These effects are mediated by recruitment and activation of the Par polarity complex and RAP1B .
PMID:20332120
Required for activation of PRKCZ and for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction .
PMID:20332120
Associates with CTNND1/p120-catenin to control CADH5 endocytosis (By similarity)
Prostaglandin G/H synthase 2
PTGS2
negative modulator
Specific functionenzyme binding
Cellular location
Microsome membrane
General function & pharmacology
Dual cyclooxygenase and peroxidase in the biosynthesis pathway of prostanoids, a class of C20 oxylipins mainly derived from arachidonate ((5Z,8Z,11Z,14Z)-eicosatetraenoate, AA, C20:4(n-6)), with a particular role in the inflammatory response .
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
Transporters(1)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Scientific references(8)
Chang D.H., Liu N., Klimek V., Hassoun H., Mazumder A., Nimer S.D., Jagannath S., Dhodapkar M.V.
Enhancement of ligand-dependent activation of human natural killer T cells by lenalidomide: therapeutic implications.
Blood
2006108(2):618-621. doi: 10.1182/blood-2005-10-4184
Anderson K.C.
Lenalidomide and Thalidomide: Mechanisms of Action—Similarities and Differences.
Seminars in Hematology
200542:S3-S8. doi: 10.1053/j.seminhematol.2005.10.001
Kotla V., Goel S., Nischal S., Heuck C., Vivek K., Das B., Verma A.
Mechanism of action of lenalidomide in hematological malignancies.
Journal Hematology Oncology
2009 Aug 122:36. doi: 10.1186/1756-8722-2-36
Qiao S.K., Guo X.N., Ren J.H., Ren H.Y.
Efficacy and Safety of Lenalidomide in the Treatment of Multiple Myeloma: A Systematic Review and Meta-analysis of Randomized Controlled Trials.
Chin Medicine Journal (Engl)
2015 May 5128(9):1215-22. doi: 10.4103/0366-6999.156134
Chen N., Wen L., Lau H., Surapaneni S., Kumar G.
Pharmacokinetics, metabolism and excretion of [(14)C]-lenalidomide following oral administration in healthy male subjects.
Cancer Chemother Pharmacology
2012 Mar69(3):789-97. doi: 10.1007/s00280-011-1760-3. Epub 2011 Oct 29
Fink E.C., Ebert B.L.
The novel mechanism of lenalidomide activity.
Blood
2015 Nov 19126(21):2366-9. doi: 10.1182/blood-2015-07-567958. Epub 2015 Oct 5
Galustian C., Dalgleish A.
Lenalidomide: a novel anticancer drug with multiple modalities.
Expert Opinion on Pharmacotherapy
2009 Jan10(1):125-33. doi: 10.1517/14656560802627903
Kiaei M., Petri S., Kipiani K., Gardian G., Choi D.K., Chen J., Calingasan N.Y., Schafer P., Muller G.W., Stewart C., Hensley K., Beal M.F.
Thalidomide and lenalidomide extend survival in a transgenic mouse model of amyotrophic lateral sclerosis.
Journal Neurosci
2006 Mar 126(9):2467-73. doi: 10.1523/JNEUROSCI.5253-05.2006
ATC classification(1 code)
ATC L04AX04
Affected organisms(1)
Humans and other mammals
International brands(2)
Salt forms(1)
Lenalidomide hydrochloride monohydrate(DBSALT003154)
Experimental properties(2)
Commercial products(248)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Lenalidomide
Additional database identifiers
Drugs Product Database (DPD)
20185
ChemSpider
187515
BindingDB
65454
HUGO Gene Nomenclature Committee (HGNC)
HGNC:30185
GeneCards
CRBN
Guide to Pharmacology
3086
UniProt Accession
CRBN_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11926
GenAtlas
TNFSF11
GeneCards
TNFSF11
GenBank Gene Database
AF013171
UniProt Accession
TNF11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11892
GenAtlas
TNF
GeneCards
TNF
GenBank Gene Database
M16441
GenBank Protein Database
339741
UniProt Accession
TNFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1764
GenAtlas
CDH5
GeneCards
CDH5
GenBank Gene Database
X79981
UniProt Accession
CADH5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
International reference pricing
4 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
From $388.00/capsule
To $411.71/capsule
Revlimid 5 mg capsule
$388.00/capsule
Revlimid 10 mg capsule
$406.05/capsule
Revlimid 15 mg capsule
$407.70/capsule
Revlimid 25 mg capsule
$411.71/capsule
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
2 active patents, 30 expired
8741929
United States
Approved 3 Jun 2014 · Expires 8 Mar 2028
1y 11m
7465800
United States
Approved 16 Dec 2008 · Expires 27 Apr 2027
1 years
7855217
United States
Approved 21 Dec 2010 · Expires 24 Nov 2024
Expired
7468363
United States
Approved 23 Dec 2008 · Expires 7 Oct 2023
Expired
7968569
United States
Approved 28 Jun 2011 · Expires 7 Oct 2023
Expired
The earliest active patent expires April 2027. Generic versions may become available after this date.
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)