製品番号: HY-A0003

レナリドミド

Name: レナリドミド
Brand: MedChemExpress
SKU: HY-A0003
Price: 66.00 USD
Availability: InStock
Rating: 5 (63 reviews)

(別名: Lenalidomide; CC-5013)

63 Cited Publications

カスタマーレビュー

Based on 63 publication(s) in Google Scholar

Lenalidomide (CC-5013) is an orally active immunomodulatory agent that binds CRBN as a molecular glue to alter substrate specificity, inducing ubiquitination and proteasome-dependent degradation of IKZF1, IKZF3 and CK1α. Lenalidomide induces apoptosis by degrading IKZF1/3, and activates p53 by degrading CK1α. Lenalidomide promotes IL-2 release and effector functions of CD8⁺ T/NK cells, while inhibiting TNF-α secretion and M1-type pyroptosis. Lenalidomide can be used in research related to hematological malignancies, acute liver failure and acute kidney injury.

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純度 : 99.94%
CAS 番号: 191732-72-6
分子式: C₁₃H₁₃N₃O₃
分子量:259.26

保管条件:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 1 year , -20°C, 6 months

Lenalidomide 構造式

CAS 番号: 191732-72-6

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生物活性
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- IC₅₀ & Target
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- 体内実験
- 臨床実験
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Publications (63)
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プロトコル (6)
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生物活性

製品説明

IC₅₀ & Target

^[1]^[3]^[4]

Cereblon

IKZF1

IKZF3

Ligands for E3 Ligase アイソフォーム固有の製品をすべて表示 :

IKZF Family アイソフォーム固有の製品をすべて表示 :

Casein Kinase アイソフォーム固有の製品をすべて表示 :

TNF Receptor アイソフォーム固有の製品をすべて表示 :

Cellular Effect

Cell Line	Type	Value	Description	References
EC9706	IC₅₀	340.3 μg/mL Compound: Lenalidomide	Antiproliferative activity against human EC9706 cells after 48 hrs by CCK-8 assay Antiproliferative activity against human EC9706 cells after 48 hrs by CCK-8 assay	[PMID: 28757066]
G-401	IC₅₀	>10 μM Compound: Lenalidomide	Inhibition of cell viability in human G-401 cells incubated for 4 days by CellTiter-Glo luminescent cell viability assay Inhibition of cell viability in human G-401 cells incubated for 4 days by CellTiter-Glo luminescent cell viability assay	[PMID: 39132814]
HCC827	IC₅₀	>10 μM Compound: Lenalidomide	Antiproliferative activity against human HCC827 cells harboring EGFRDel19 mutant assessed as reduction in cell viability incubated for 72 hrs by MTT assay Antiproliferative activity against human HCC827 cells harboring EGFRDel19 mutant assessed as reduction in cell viability incubated for 72 hrs by MTT assay	[PMID: 31951960]
HEK293	IC₅₀	5.19 μM Compound: Lenalidomide	Inhibition of BRD4 bromodomain 2 (unknown origin) in HEK293 cells cotransfected with eGFP by flow cytometry based mCherry reporter gene analysis Inhibition of BRD4 bromodomain 2 (unknown origin) in HEK293 cells cotransfected with eGFP by flow cytometry based mCherry reporter gene analysis	[PMID: 32550984]
JeKo-1	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human JeKo1 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human JeKo1 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
JeKo-1	IC₅₀	>20000 nM Compound: Lenalidomide	Antiproliferative activity against human Jeko-1 cells expressing CRBN-knockout assessed as cell viability measured after 7 days by CCK-8 assay Antiproliferative activity against human Jeko-1 cells expressing CRBN-knockout assessed as cell viability measured after 7 days by CCK-8 assay	[PMID: 35635954]
JeKo-1	IC₅₀	>20000 nM Compound: Lenalidomide	Antiproliferative activity against human Jeko-1 cells assessed as cell viability measured after 7 days by CCK-8 assay Antiproliferative activity against human Jeko-1 cells assessed as cell viability measured after 7 days by CCK-8 assay	[PMID: 35635954]
K562	IC₅₀	>10 μM Compound: Lenalidomide	Antiproliferative activity against human K562 cells assessed as cell growth inhibition measured after 48 hrs by CCK8 assay Antiproliferative activity against human K562 cells assessed as cell growth inhibition measured after 48 hrs by CCK8 assay	[PMID: 34217059]
K562	IC₅₀	>10 μM Compound: Lenalidomide	Antiproliferative activity against human K562 cells assessed as inhibition of cell growth incubated for 2 days by CCK8 assay Antiproliferative activity against human K562 cells assessed as inhibition of cell growth incubated for 2 days by CCK8 assay	[PMID: 36306539]
Kasumi 1	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human Kasumi-1 cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human Kasumi-1 cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
MCF-10A	IC₅₀	>20 μM Compound: Lenalidomide	Cytotoxicity against human MCF10A cells after 72 hrs by MTS assay Cytotoxicity against human MCF10A cells after 72 hrs by MTS assay	[PMID: 29795767]
MCF7	IC₅₀	>100 μM Compound: Len	Antiproliferative activity against human MCF7 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay Antiproliferative activity against human MCF7 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay	[PMID: 37619298]
MDA-MB-231	IC₅₀	>100 μM Compound: Len	Antiproliferative activity against human MDA-MB-231 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay Antiproliferative activity against human MDA-MB-231 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay	[PMID: 37619298]
MDA-MB-468	IC₅₀	>100 μM Compound: Len	Antiproliferative activity against human MDA-MB-468 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay Antiproliferative activity against human MDA-MB-468 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay	[PMID: 37619298]
MM.1S	IC₅₀	50 nM Compound: 1	Antiproliferative activity against human MM1S cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human MM1S cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
MM.1S	IC₅₀	0.081 μM Compound: Lenalidoamide	Antiproliferative activity against human MM1.S cells assessed as reduction in cell growth measured after 7 days culturing by CellTiter 96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human MM1.S cells assessed as reduction in cell growth measured after 7 days culturing by CellTiter 96 Aqueous non-radioactive cell proliferation assay	[PMID: 33328101]
MM.1S	IC₅₀	70.17 nM Compound: Lenalidomide	Antiproliferative activity against human MM1.S cells assessed as cell viability measured after 7 days by CCK-8 assay Antiproliferative activity against human MM1.S cells assessed as cell viability measured after 7 days by CCK-8 assay	[PMID: 35635954]
MM.1S	IC₅₀	>20000 nM Compound: Lenalidomide	Antiproliferative activity against human MM1.S cells assessed as cell viability measured after 3 days by CCK-8 assay Antiproliferative activity against human MM1.S cells assessed as cell viability measured after 3 days by CCK-8 assay	[PMID: 35635954]
MV4-11	IC₅₀	>20000 nM Compound: Lenalidomide	Antiproliferative activity against human MV411 cells after 72 hrs by MTS assay Antiproliferative activity against human MV411 cells after 72 hrs by MTS assay	[PMID: 29795767]
MV4-11	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human MV411 cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human MV411 cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
MX1	IC₅₀	>100 μM Compound: Len	Antiproliferative activity against human MX1 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay Antiproliferative activity against human MX1 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay	[PMID: 37619298]
NAMALVA	IC₅₀	0.36 μM Compound: 1	Antiproliferative activity against human NAMALWA cells assessed as inhibition of [3H]thymidine incorporation after 72 hrs by scintillation counting Antiproliferative activity against human NAMALWA cells assessed as inhibition of [3H]thymidine incorporation after 72 hrs by scintillation counting	[PMID: 23168019]
PBMC	IC₅₀	0.1 μM Compound: 1	Inhibition of TNF-alpha production in LPS-stimulated human PBMC preincubated for 1 hr before LPS challenge measured after 28 to 20 hrs by ELISA Inhibition of TNF-alpha production in LPS-stimulated human PBMC preincubated for 1 hr before LPS challenge measured after 28 to 20 hrs by ELISA	[PMID: 23168019]
PBMC	IC₅₀	100 nM Compound: 1	Antiinflammatory activity in human PBMC cells assessed as reduction in LPS-induced TNF-alpha production preincubated for 1 hr followed by LPS addition and measured after 18 to 20 hrs by ELISA Antiinflammatory activity in human PBMC cells assessed as reduction in LPS-induced TNF-alpha production preincubated for 1 hr followed by LPS addition and measured after 18 to 20 hrs by ELISA	[PMID: 31125896]
PBMC	IC₅₀	>20000 nM Compound: 1	Cytotoxicity against human PBMC cells by CellTiter96 Aqueous non-radioactive cell proliferation assay Cytotoxicity against human PBMC cells by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
PBMC	IC₅₀	100 nM Compound: 11; CC-5013	Inhibition of TNF-alpha release in LPS stimulated human PBMC Inhibition of TNF-alpha release in LPS stimulated human PBMC	[PMID: 33906050]
Raji	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human Raji cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human Raji cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
RPMI-8226	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human RPMI8226 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human RPMI8226 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
T-cell	EC₅₀	0.15 μM Compound: 1	Inhibition of IL-2 production in human T cells measured after 2 to 3 days by ELISA Inhibition of IL-2 production in human T cells measured after 2 to 3 days by ELISA	[PMID: 23168019]
THP-1	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human THP1 cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human THP1 cells measured after 168 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
U-266	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human U266 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human U266 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]
WI-38	IC₅₀	>20 μM Compound: Lenalidomide	Cytotoxicity against human WI38 cells after 72 hrs by MTS assay Cytotoxicity against human WI38 cells after 72 hrs by MTS assay	[PMID: 29795767]
Z-138	IC₅₀	>20000 nM Compound: 1	Antiproliferative activity against human Z138 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay Antiproliferative activity against human Z138 cells measured after 72 hrs by CellTiter96 Aqueous non-radioactive cell proliferation assay	[PMID: 31125896]

体外実験

Lenalidomide (1-10 μM; 4-24 h) induces ubiquitination and degradation of CK1α in human del (5q) myeloid KG-1 cells^[1].
Lenalidomide (0.01-10 μM; 0-24 h) induces CRBN-dependent post-translational degradation of CK1α in multiple human hematopoietic cell lines^[1].
Lenalidomide (1-10 μM; 90 min-4 h) mediates the physical interaction between CK1α and CRBN, thereby enabling CRL4^CRBN-dependent ubiquitination of CK1α in human hematopoietic cells and cell-free systems^[1].
Lenalidomide (1 μM; 5-25 days) specifically depletes CD34⁺ cells derived from patients with del (5q) myelodysplastic syndrome (MDS), and this effect is reversed by CSNK1A1 overexpression; in contrast, CSNK1A1 downregulation sensitizes primary human CD34⁺ hematopoietic stem/progenitor cells to Lenalidomide^[1].
Lenalidomide (0.01-10 μM; 4-24 h) induces the degradation of CK1α, IKZF1 and IKZF3 in mouse Ba/F3 cells carrying the mouse Crbn I391V mutation and human 293T cells^[1].
Lenalidomide (0.3-10 μM; 6-72 h) selectively induces the degradation of CK1α in human MDS-L and KG-1 myeloid cells, and this effect is blocked by competition with the cereblon modulator CC-122 (HY-100507)^[1].
Lenalidomide selectively destabilizes exogenous IKZF1 and IKZF3 (but not other Ikaros family members or IRF4) in a proteasome-dependent and cullin-dependent manner in 293FT embryonic kidney cells^[4].
Lenalidomide induces proteasomal degradation of endogenous IKZF1 (in U937 leukemia cells) as well as endogenous IKZF1 and IKZF3 (in MM1S and L363 myeloma cells) via a post-transcriptional, cullin-dependent mechanism^[4].
Lenalidomide-induced degradation of IKZF1 and IKZF3 in 293FT embryonic kidney cells, U937 leukemia cells, and MM1S, L363 and KMS34 myeloma cells is strictly dependent on functional cereblon^[4].
Lenalidomide mediates direct and specific interactions between cereblon and IKZF1/IKZF3, thereby triggering cereblon-dependent ubiquitination of IKZF1^[4].
Lenalidomide exerts antiproliferative effects on MM1S, KMS34 and L363 myeloma cells via cereblon-dependent degradation of IKZF1 and IKZF3, and this mechanism is both necessary and sufficient for its anti-myeloma activity^[4].
Lenalidomide inhibits the TNF-α/HMGB1 pathway and reduces the pyroptosis level of THP-1 M1 macrophages differentiated by PMA and induced by LPS (HY-D1056)^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

Western Blot Analysis^[1]

View Protocol

Cell Line:

human del(5q) myeloid KG-1 cells, human multiple myeloma MM1S cells, human chronic myelogenous leukemia K562 cells, human T-cell leukemia Jurkat cells, human embryonic kidney 293T cells
Concentration:

1 μM (KG-1 cells); 0.01, 0.1, 1 and 10 μM (MM1S, K562, Jurkat cells); 10 μM (293T cells)
Incubation Time:

0, 1, 2, 3, 5, 8, 24 h (KG-1 cells); 24 h (MM1S, K562, Jurkat cells); 5 h (293T cells)
Result:

Caused time-dependent decreases in CK1α protein levels in KG-1 cells, with visible reduction by 2 hours and near-complete loss by 24 hours at 1 μM.
Decreased CK1α levels in MM1S, K562, and Jurkat cells, with no effect on CSNK1A1 mRNA expression at 0.01-10 μM for 24 h.
Eliminated lenalidomide-dependent CK1α degradation in 293T cells with homozygous CRBN inactivation at 10 μM for 5 h.

体内実験

Lenalidomide (10 mg/kg; i.p.; daily; 14 days) does not reduce CK1α protein levels in the bone marrow of wild-type C57BL/6 mice^[1].
Lenalidomide (0.5-45 mg/kg; i.v., i.p., p.o.; single bolus) is well-tolerated at doses up to 15 mg/kg i.v., 22.5 mg/kg i.p., and 45 mg/kg p.o. in healthy ICR mice, with preferential distribution to lung, liver, heart, and spleen, and limited brain penetration detectable only at i.v. doses of 5 mg/kg and higher^[5].
Lenalidomide (50 mg/kg; p.o.; daily; 21 days starting on day +14 after transplantation) synergizes with anti-TIGIT to induce CD8⁺ T cell-dependent antimyeloma activity, reduce T cell exhaustion, and expand memory T cells in the bone marrow of multiple myeloma-bearing mice after autologous stem cell transplantation; lenalidomide monotherapy shows no antimyeloma activity with suboptimal T cell dosing^[2].
Lenalidomide (3 mg/kg; i.p.; single dose) reduces pathological damage, improves organ function, inhibits TNF-α/HMGB1 pathway activation, suppresses pyroptosis, and reduces M1 macrophage activation in mice with LPS/D-Gal-induced ALF and AKI^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C57BL/6 (female)^[1]
Dosage:

10 mg/kg
Administration:

i.p.; daily; 14 days
Result:

Did not alter CK1α protein levels in mouse bone marrow cells.

Animal Model:

C57BL/6J; CRBN (female, 8-12 weeks of age, multiple myeloma model via Vk12653 myeloma cell injection 2 weeks prior to autologous stem cell transplantation with suboptimal donor T cell dose)^[2]
Dosage:

50 mg/kg
Administration:

p.o.; daily; 21 days starting on day +14 after transplantation
Result:

Showed no antimyeloma activity as monotherapy with suboptimal T cell dose.
Drove synergistic antimyeloma efficacy in combination with anti-TIGIT.
Reduced serum M-band progression in combination with anti-TIGIT.
Improved survival in combination with anti-TIGIT.
Reduced the frequency of exhausted CD8+ T cells in combination with anti-TIGIT.
Expanded central memory CD8+ T cell subsets in combination with anti-TIGIT.
Enhanced IFN-γ production from PD-1+ CD8+ T cells in combination with anti-TIGIT.
Increased expression of Il7r and Ikzf2 genes associated with memory T cell maintenance in bone marrow CD8+ T cells in combination with anti-TIGIT.
Fully protected long-term survivors against myeloma rechallenge in combination with anti-TIGIT.

Animal Model:

C57/BL6 (male, 8-10 weeks old, 20-25 g, LPS and D-Gal induced)^[3]
Dosage:

3 mg/kg
Administration:

i.p.; single dose (2 hours before LPS/D-Gal exposure)
Result:

Reduced liver lobular structural damage, hepatocyte necrosis, and inflammatory cell infiltration in liver tissue.
Ameliorated renal tubular epithelial swelling, brush border loss, and vacuolar degeneration in kidney tissue.
Decreased serum levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, blood urea nitrogen, creatinine, TNF-α, HMGB1, IL-1β, and IL-18 compared to the model group.
Decreased protein levels of IL-1β, IL-18, NLRP3, caspase-1 p10+p12, and GSDMD in liver and kidney tissues.
Reduced expression of M1 macrophage markers CD68 and iNOS in liver and kidney tissues.

Animal Model:

ICR mice (8-10 weeks of age)^[5]
Dosage:

0.5、1.5、5、10、15 mg/kg (i.v.);
0.5、10、22.5 mg/kg (i.p.);
45 mg/kg (p.o.)
Administration:

i.v.; single bolus; i.p.; single bolus; p.o.; single bolus
Result:

Caused no observable toxicity up to 24 hours post-dose at 15 mg/kg i.v., 22.5 mg/kg i.p., and 45 mg/kg p.o., with one fatal event occurring immediately after 15 mg/kg i.v. administration.
Reached highest tissue concentrations at 2 minutes post-10 mg/kg i.v. dose in lung (15 μg/g), followed by liver (5 μg/g), heart (2.4 μg/g), and spleen (1.3 μg/g).
Decreased to less than 15 ng/g in all tissues by 8 hours post-10 mg/kg i.v. dose.
Was detectable in brain tissue only after i.v. doses of 5 and 10 mg/kg.

臨床実験

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

化学情報

CAS 番号 191732-72-6
性状 Solid
分子量 259.26
分子式 C₁₃H₁₃N₃O₃
Color Off-white to light yellow
SMILES

O=C1C2=CC=CC(N)=C2CN1C(C(N3)=O)CCC3=O
別名

Lenalidomide; CC-5013
輸送条件

Room temperature in continental US; may vary elsewhere.

保管条件

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	1 year
	-20°C	6 months

Publications (63)

All WB

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Journal Impact Factor

Nature

Fate induction in CD8 CAR T cells through asymmetric cell division. [Abstract]

2024 Sep;633(8030):670-677. PMID: 39198645
Cancer Cell

High-performance multiplex drug-gated CAR circuits. [Abstract]

2022 Nov 14;40(11):1294-1305.e4. PMID: 36084652
Cell

Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models. [Abstract]

2018 Sep 20;175(1):171-185.e25. PMID: 30146162

Lenalidomide purchased from MedChemExpress. Usage Cited in: Cell. 2018 Sep 20;175(1):171-185.e25. [Abstract]

WB analysis of MV4-11 cells treated for 6.5 hr with Lenalidomide, BTX161, A51, or A86 at the indicated concentrations or DMSO.
Nat Cancer

IKAROS and MENIN coordinate therapeutically actionable leukemogenic gene expression in MLL-r acute myeloid leukemia. [Abstract]

2022 May;3(5):595-613. PMID: 35534777

Lenalidomide purchased from MedChemExpress. Usage Cited in: Nat Cancer. 2022 May;3(5):595-613. [Abstract]

Western blot analysis for IKAROS, CK1α and MENIN protein following treatment of MV4;11 human MLL-r AML cell line for 5 hours with increasing doses of Thalidomide, lenalidomide, Pomalidomide and iberdomide (10,100, 1000 nM), using ACTIN as a loading control.
Cancer Res

Targeted Degradation of SOS1 Exhibits Potent Anticancer Activity and Overcomes Resistance in KRAS-Mutant Tumors and BCR-ABL-Positive Leukemia. [Abstract]

2025 Jan 2;85(1):101-117. PMID: 39437162
Nat Commun

Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation. [Abstract]

2026 Feb 12;17(1):1493. PMID: 41680163
Nat Commun

PROTAC repurposing uncovers a noncanonical binding surface that mediates chemical degradation of nuclear receptors. [Abstract]

2025 Nov 6;16(1):9805. PMID: 41198675
Nat Commun

Multiple myeloma associated long non-coding RNA PLUM confers chemoresistance by enhancing PRC2 mediated UPR pathway activation. [Abstract]

2025 Sep 1;16(1):8155. PMID: 40890111
Nat Commun

pSILAC mass spectrometry reveals ZFP91 as IMiD-dependent substrate of the CRL4CRBN ubiquitin ligase. [Abstract]

2017 May 22:8:15398. PMID: 28530236

Lenalidomide purchased from MedChemExpress. Usage Cited in: Nat Commun. 2017 May 22:8:15398. [Abstract]

HEK293T cells are treated with 50 μg/mL Cycloheximide and increasing concentrations of Lenalidomide, Thalidomide or with DMSO, and cells are incubated for 6 h. ZFP91 and GAPDH levels are detected using anti-ZFP91 or anti-GAPDH immunoblotting.
Nat Chem Biol

Acute pharmacological degradation of Helios destabilizes regulatory T cells. [Abstract]

2021 Jun;17(6):711-717. PMID: 34035522
Microbiome

Microbiota-derived urolithin A in monoclonal gammopathies and multiple myeloma therapy. [Abstract]

2025 Feb 28;13(1):56. PMID: 40022244
Adv Sci (Weinh)

Targeting PRKCN, an Essential Driver Orchestrating mTOR-IRF4 Axis Independently of Kinase Activity, in Multiple Myeloma. [Abstract]

2026 Apr;13(21):e18975. PMID: 41655233
Cell Rep Med

CAN-Scan: A multi-omic phenotype-driven precision oncology platform identifies prognostic biomarkers of therapy response for colorectal cancer. [Abstract]

2025 Apr 15;6(4):102053. PMID: 40187357
Cell Rep Med

STAT3 couples activated tyrosine kinase signaling to the oncogenic core transcriptional regulatory circuitry of anaplastic large cell lymphoma. [Abstract]

2024 Mar 19;5(3):101472. PMID: 38508140
Cell Commun Signal

IKZF1 as a potential therapeutic target for dendritic cell-mediated immunotherapy in IgA nephropathy. [Abstract]

2025 May 7;23(1):216. PMID: 40336063
Acta Pharmacol Sin

Targeting the HuR/E2F7 axis synergizes with bortezomib against multiple myeloma. [Abstract]

2025 Mar 25. PMID: 40133626
Acta Pharmacol Sin

The novel cereblon modulator CC-885 inhibits mitophagy via selective degradation of BNIP3L. [Abstract]

2020 Sep;41(9):1246-1254. PMID: 32210356
J Transl Med

Doxorubicin synergizes bortezomib-induced multiple myeloma cell death by inhibiting aggresome formation and augmenting endoplasmic reticulum/Golgi stress and apoptosis. [Abstract]

2024 Dec 3;22(1):1095. PMID: 39623468
Leukemia

Targeting ABCD1-ACOX1-MET/IGF1R axis suppresses multiple myeloma. [Abstract]

2025 Mar;39(3):720-733. PMID: 39885295
Int J Biol Macromol

2026 Jan 7;340:150099.
Mol Ther Oncol

Dual CARM1-and IKZF3-targeting: A novel approach to multiple myeloma therapy synergy between CARM1 inhibition and IMiDs. [Abstract]

2025 Feb 20;33(1):200952. PMID: 40123976
Free Radic Biol Med

Targeting ABCB6 with nitidine chloride inhibits PI3K/AKT signaling pathway to promote ferroptosis in multiple myeloma. [Abstract]

2023 Jul:203:86-101. PMID: 37044150
Cell Rep

Identification of WNK1 as a therapeutic target to suppress IgH/MYC expression in multiple myeloma. [Abstract]

2024 May 8;43(5):114211. PMID: 38722741
Cell Syst

A Library of Phosphoproteomic and Chromatin Signatures for Characterizing Cellular Responses to Drug Perturbations. [Abstract]

2018 Apr 25;6(4):424-443.e7. PMID: 29655704
J Med Chem

Real-Time NanoBRET Target Engagement Reveals Permeability-Activity Relationships in BET-Targeting Degraders. [Abstract]

2026 May 28;69(10):12669-12677. PMID: 42139371
Cell Rep Methods

RECOVER identifies synergistic drug combinations in vitro through sequential model optimization. [Abstract]

2023 Oct 23;3(10):100599. PMID: 37797618
Eur J Pharmacol

Doxorubicin-mediated retardation of aggresome formation enhances Carfilzomib-induced cell death synergistically by augmenting ER stress and proapoptotic signaling. [Abstract]

2025 Dec 5:1008:178303. PMID: 41183585
Int Immunopharmacol

Pomalidomide promotes macrophage control of Mycobacterium tuberculosis via enhancing HDAC6-mediated autophagy. [Abstract]

2025 Jun 17:158:114831. PMID: 40373598
Int J Mol Sci

Lenalidomide Promotes Thrombosis Formation, but Does Not Affect Platelet Activation in Multiple Myeloma. [Abstract]

2023 Sep 14;24(18):14097. PMID: 37762399
Front Cell Infect Microbiol

Lenalidomide potentially reduced the level of cell- associated HIV RNA and improved persistent inflammation in patients with HIV-associated cryptococcal meningitis a pilot study. [Abstract]

2022 Jul 28;12:954814. PMID: 35967862
Inflammation

Progranulin Promotes Regeneration of Inflammatory Periodontal Bone Defect in Rats via Anti-inflammation, Osteoclastogenic Inhibition, and Osteogenic Promotion. [Abstract]

2019 Feb;42(1):221-234. PMID: 30187338
ACS Omega

Dynamic Detection of the E3-PROTAC-Target Protein Ternary Complex In Vitro and In Vivo via Bimolecular Fluorescence Complementation. [Abstract]

2024 Dec 3;9(50):49739-49748. PMID: 39713624
Biochim Biophys Acta Mol Basis Dis

Dengue virus is involved in insulin resistance via the downregulation of IRS-1 by inducing TNF-α secretion. [Abstract]

2022 Oct 1;1868(10):166472. PMID: 35752384
Cancer Sci

Activity of TAS4464, a novel NEDD8 activating enzyme E1 inhibitor, against multiple myeloma via inactivation of nuclear factor κB pathways. [Abstract]

2019 Dec;110(12):3802-3810. PMID: 31583781
Am J Pathol

Pathophysiological function of endogenous calcitonin gene-related peptide in ocular vascular diseases. [Abstract]

2015 Jun;185(6):1783-94. PMID: 25857228
Neoplasia

Cholesterol biosynthesis as a drug-induced vulnerability in diffuse large B cell lymphoma insensitive to EZH2 inhibition. [Abstract]

2025 Oct 27:70:101243. PMID: 41151153
Cancers (Basel)

Synergy between BRD9- and IKZF3-Targeting as a Therapeutic Strategy for Multiple Myeloma. [Abstract]

2024 Mar 28;16(7):1319. PMID: 38610997
Oncol Rep

Microvesicles shed from bortezomib-treated or lenalidomide-treated human myeloma cells inhibit angiogenesis in vitro. [Abstract]

2018 Jun;39(6):2873-2880. PMID: 29693175

Lenalidomide purchased from MedChemExpress. Usage Cited in: Oncol Rep. 2018 Jun;39(6):2873-2880. [Abstract]

Representative western blot membranes showing the expression levels of NF-κB p-p65 and H3 in nuclear protein and of NF-κB p65 and β-actin in total protein. β-actin and H3 are used as internal controls.
iScience

Identification of a drug-response gene in multiple myeloma through longitudinal single-cell transcriptome sequencing. [Abstract]

2022 Jul 19;25(8):104781. PMID: 35992084
Bioengineering (Basel)

Precision Oncology for High-Grade Gliomas: A Tumor Organoid Model for Adjuvant Treatment Selection. [Abstract]

2025 Oct 19;12(10):1121. PMID: 41155119
Clin Chim Acta

Detection of lenalidomide metabolites in urine to discover drug-resistant compounds. [Abstract]

2024 Jan 15:553:117707. PMID: 38103853
ACS Pharmacol Transl Sci

General Stepwise Approach to Optimize a TR-FRET Assay for Characterizing the BRD/PROTAC/CRBN Ternary Complex. [Abstract]

2021 Feb 26;4(2):941-952. PMID: 33860212
Cancer Med

Synergistic Antitumor Activity of HAT Inhibitor A485 and XPO1 Inhibitor KPT8602 in Multiple Myeloma. [Abstract]

2026 Jun;15(6):e71985. PMID: 42231094
Exp Cell Res

Network-based analysis with primary cells reveals drug response landscape of acute myeloid leukemia. [Abstract]

2020 Aug 1;393(1):112054. PMID: 32376287
Food Chem Toxicol

Inorganic arsenic induces pyroptosis and pancreatic β cells dysfunction through stimulating the IRE1α/TNF-α pathway and protective effect of taurine. [Abstract]

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SSRN

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bioRxiv

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Lenalidomide purchased from MedChemExpress. Usage Cited in: Elife. 2018 Aug 1:7:e38430. [Abstract]

H9 hESC are treated with increasing concentrations of Thalidomide, Lenalidomide, Pomalidomide, or DMSO as a control. Following 24 h of incubation, SALL4 and GAPDH protein levels are assessed by western blot analysis.
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溶剤 & 溶解度

体外:

DMSO : 100 mg/mL (385.71 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.8571 mL

19.2857 mL

38.5713 mL

5 mM

0.7714 mL

3.8571 mL

7.7143 mL

10 mM

0.3857 mL

1.9286 mL

3.8571 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

モル濃度計算機

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

濃度濃度

体積体積

分子量分子量

希釈計算機

濃度 _(開始) × 体積 _(開始) = 濃度 _(終了) × 体積 _(終了)

濃度 _(開始) 濃度 _(開始)

体積 _(開始) 体積 _(開始)

濃度 _(終了) 濃度 _(終了)

体積 _(終了) 体積 _(終了)

体内:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (9.64 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (9.64 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (9.64 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

プロトコル

All Cell Biology Animals and Diseases Signal Pathway Related

Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
Nephrotoxicity Study
This protocol assesses nephrotoxicity by combining functional kidney injury readouts, urinary/tissue injury biomarkers, and renal histopathology. Serum creatinine and BUN reflect impaired kidney function, while KIM-1, NGAL, clusterin, osteopontin, IL-18, cystatin C, nephrin, Oat5, urinary protein, glucose, and alkaline phosphatase have been used to detect tubular injury in cisplatin-, gentamicin-, and acetaminophen-induced nephrotoxicity models.
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam

純度とドキュメンテーション

バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

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COA (2659 KB)
元素分析報告書 (2659 KB)
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参考文献

[1]. Krönke J, et al. Lenalidomide induces ubiquitination and degradation of CK1α in del(5q) MDS. Nature. 2015 Jul 9;523(7559):183-188. [Content Brief]

[2]. Minnie SA, et al. TIGIT inhibition and lenalidomide synergistically promote antimyeloma immune responses after stem cell transplantation in mice. The Journal of clinical investigation. 2023 Feb 15;133(4):e157907. [Content Brief]

[3]. Wang Y, et al. TNF-α/HMGB1 inflammation signalling pathway regulates pyroptosis during liver failure and acute kidney injury. Cell Prolif. 2020 Jun;53(6):e12829. [Content Brief]

[4]. Lu G, et al. The myeloma drug lenalidomide promotes the cereblon-dependent destruction of Ikaros proteins. Science (New York, N.Y.). 2014 Jan 17;343(6168):305-9. [Content Brief]

[5]. Rozewski DM, et al. Pharmacokinetics and tissue disposition of lenalidomide in mice. The AAPS journal. 2012 Dec;14(4):872-82. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.8571 mL	19.2857 mL	38.5713 mL	96.4283 mL
	5 mM	0.7714 mL	3.8571 mL	7.7143 mL	19.2857 mL
	10 mM	0.3857 mL	1.9286 mL	3.8571 mL	9.6428 mL
	15 mM	0.2571 mL	1.2857 mL	2.5714 mL	6.4286 mL
	20 mM	0.1929 mL	0.9643 mL	1.9286 mL	4.8214 mL
	25 mM	0.1543 mL	0.7714 mL	1.5429 mL	3.8571 mL
	30 mM	0.1286 mL	0.6429 mL	1.2857 mL	3.2143 mL
	40 mM	0.0964 mL	0.4821 mL	0.9643 mL	2.4107 mL
	50 mM	0.0771 mL	0.3857 mL	0.7714 mL	1.9286 mL
	60 mM	0.0643 mL	0.3214 mL	0.6429 mL	1.6071 mL
	80 mM	0.0482 mL	0.2411 mL	0.4821 mL	1.2054 mL
	100 mM	0.0386 mL	0.1929 mL	0.3857 mL	0.9643 mL

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