Lenalidomide hemihydrate
Based on 64 publication(s) in Google Scholar
Lenalidomide hemihydrate (CC-5013 hemihydrate) 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 hemihydrate induces apoptosis by degrading IKZF1/3, and activates p53 by degrading CK1α. Lenalidomide hemihydrate promotes IL-2 release and effector functions of CD8+ T/NK cells, while inhibiting TNF-α secretion and M1-type pyroptosis. Lenalidomide hemihydrate can be used in research related to hematological malignancies, acute liver failure and acute kidney injury.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 99.98%
- CAS. Nr.: 847871-99-2
- Formel: C13H14N3O3.5
- Molecular Weight:268.27
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Speicherung:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
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HY-A0003
LenalidomideImmunomodulator -
HY-10984
PomalidomideImmunomodulatory Agent -
HY-14658
ThalidomideCereblon Inhibitor -
HY-10227
BortezomibProteasome Inhibitor -
HY-N0219
BicucullineGABAA Receptor Antagonist -
HY-19568
PeficitinibJAK Inhibitor -
HY-50895
GefitinibEGFR Inhibitor -
HY-15760
Necrostatin-1RIPK1 Inhibitor -
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Lenalidomide (Standard)Reference Standard -
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Publications Citing Use of MedChemExpress (MCE) Lenalidomide hemihydrate
More- Nature. 2024 Sep;633(8030):670-677. [Abstract]
- Cancer Cell. 2022 Nov 14;40(11):1294-1305.e4. [Abstract]
- Cell. 2018 Sep 20;175(1):171-185.e25. [Abstract]
- Nat Cancer. 2022 May;3(5):595-613. [Abstract]
- Cancer Res. 2025 Jan 2;85(1):101-117. [Abstract]
- Nat Commun. 2026 Feb 12;17(1):1493. [Abstract]
- Nat Commun. 2025 Nov 6;16(1):9805. [Abstract]
- Nat Commun. 2025 Sep 1;16(1):8155. [Abstract]
- Nat Commun. 2017 May 22:8:15398. [Abstract]
- Nat Chem Biol. 2021 Jun;17(6):711-717. [Abstract]
- Microbiome. 2025 Feb 28;13(1):56. [Abstract]
- Adv Sci (Weinh). 2026 Apr;13(21):e18975. [Abstract]
- Cell Rep Med. 2025 Apr 15;6(4):102053. [Abstract]
- Cell Rep Med. 2024 Mar 19;5(3):101472. [Abstract]
- Cell Death Dis. 2026 Aug 6.
- Cell Commun Signal. 2025 May 7;23(1):216. [Abstract]
- Acta Pharmacol Sin. 2025 Mar 25. [Abstract]
- Acta Pharmacol Sin. 2020 Sep;41(9):1246-1254. [Abstract]
- J Transl Med. 2024 Dec 3;22(1):1095. [Abstract]
- Leukemia. 2025 Mar;39(3):720-733. [Abstract]
- Int J Biol Macromol. 2026 Jan 7;340:150099.
- Mol Ther Oncol. 2025 Feb 20;33(1):200952. [Abstract]
- Free Radic Biol Med. 2023 Jul:203:86-101. [Abstract]
- Cell Rep. 2024 May 8;43(5):114211. [Abstract]
- Cell Syst. 2018 Apr 25;6(4):424-443.e7. [Abstract]
- J Med Chem. 2026 May 28;69(10):12669-12677. [Abstract]
- Cell Rep Methods. 2023 Oct 23;3(10):100599. [Abstract]
- Eur J Pharmacol. 2025 Dec 5:1008:178303. [Abstract]
- Int Immunopharmacol. 2025 Jun 17:158:114831. [Abstract]
- Int J Mol Sci. 2023 Sep 14;24(18):14097. [Abstract]
- Front Cell Infect Microbiol. 2022 Jul 28;12:954814. [Abstract]
- Inflammation. 2019 Feb;42(1):221-234. [Abstract]
- ACS Omega. 2024 Dec 3;9(50):49739-49748. [Abstract]
- Biochim Biophys Acta Mol Basis Dis. 2022 Oct 1;1868(10):166472. [Abstract]
- Cancer Sci. 2019 Dec;110(12):3802-3810. [Abstract]
- Am J Pathol. 2015 Jun;185(6):1783-94. [Abstract]
- Neoplasia. 2025 Oct 27:70:101243. [Abstract]
- Cancers (Basel). 2024 Mar 28;16(7):1319. [Abstract]
- Oncol Rep. 2018 Jun;39(6):2873-2880. [Abstract]
- iScience. 2022 Jul 19;25(8):104781. [Abstract]
- Bioengineering (Basel). 2025 Oct 19;12(10):1121. [Abstract]
- Clin Chim Acta. 2024 Jan 15:553:117707. [Abstract]
- ACS Pharmacol Transl Sci. 2021 Feb 26;4(2):941-952. [Abstract]
- Cancer Med. 2026 Jun;15(6):e71985. [Abstract]
- Exp Cell Res. 2020 Aug 1;393(1):112054. [Abstract]
- Food Chem Toxicol. 2019 Mar:125:392-402. [Abstract]
- SSRN. 2026 Jun 16.
- Charles University. 2026.
- bioRxiv. 2026 Feb 8:2026.02.06.704516. [Abstract]
- Chemrxiv. 2025 Nov 17.
- Harvard University. 2025.
- bioRxiv. 2024 October 19.
- Patent. US20240261246A1.
- bioRxiv. 2024 June 12.
- Universidad de Navarra. 2024 Feb 28.
- Patent. US20220332776A1.
- Oxid Med Cell Longev. 2021 Dec 29:2021:8302831. [Abstract]
- Patent. US20210379039A1.
- University of Washington. 2021 Aug 31.
- bioRxiv. April.
- Patent. US20180263995A1.
- Elife. 2018 Aug 1:7:e38430. [Abstract]
- Patent. US20170360780A1.
- Masaryk University. 2014.
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Alle TNF Receptor Isoform-spezifische Produkte anzeigen
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Biologische Aktivität
Beschreibung
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Cereblon |
IKZF1 |
IKZF3 |
In Vitro
Lenalidomide (1-10 μM; 4-24 h) hemihydrate induces ubiquitination and degradation of CK1α in human del (5q) myeloid KG-1 cells[1].
Lenalidomide (0.01-10 μM; 0-24 h) hemihydrate induces CRBN-dependent post-translational degradation of CK1α in multiple human hematopoietic cell lines[1].
Lenalidomide (1-10 μM; 90 min-4 h) hemihydrate mediates the physical interaction between CK1α and CRBN, thereby enabling CRL4CRBN-dependent ubiquitination of CK1α in human hematopoietic cells and cell-free systems[1].
Lenalidomide (1 μM; 5-25 days) hemihydrate 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 hemihydrate[1].
Lenalidomide (0.01-10 μM; 4-24 h) hemihydrate 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) hemihydrate 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 hemihydrate 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 hemihydrate 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 hemihydrate-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 hemihydrate mediates direct and specific interactions between cereblon and IKZF1/IKZF3, thereby triggering cereblon-dependent ubiquitination of IKZF1[4].
Lenalidomide hemihydrate 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 hemihydrate 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.
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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
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Concentration:1 μM (KG-1 cells); 0.01, 0.1, 1 and 10 μM (MM1S, K562, Jurkat cells); 10 μM (293T cells)
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Incubation Time:0, 1, 2, 3, 5, 8, 24 h (KG-1 cells); 24 h (MM1S, K562, Jurkat cells); 5 h (293T cells)
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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.
In Vivo
Lenalidomide (0.5-45 mg/kg; i.v., i.p., p.o.; single bolus) hemihydrate 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) hemihydrate 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 hemihydrate monotherapy shows no antimyeloma activity with suboptimal T cell dosing[2].
Lenalidomide (3 mg/kg; i.p.; single dose) hemihydrate 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.
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Animal Model:C57BL/6 (female)[1]
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Dosage:10 mg/kg
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Administration:i.p.; daily; 14 days
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Result:Did not alter CK1α protein levels in mouse bone marrow cells.
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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]
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Dosage:50 mg/kg
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Administration:p.o.; daily; 21 days starting on day +14 after transplantation
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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.
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Animal Model:C57/BL6 (male, 8-10 weeks old, 20-25 g, LPS and D-Gal induced)[3]
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Dosage:3 mg/kg
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Administration:i.p.; single dose (2 hours before LPS/D-Gal exposure)
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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.
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Animal Model:ICR mice (8-10 weeks of age)[5]
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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
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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.
Chemical Information
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CAS. Nr. 847871-99-2
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Appearance Solid
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Molecular Weight 268.27
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Formel C13H14N3O3.5
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Color Off-white to pink
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SMILES
O=C1N(C2C(NC(CC2)=O)=O)CC3=C(N)C=CC=C31.[0.5 H2O]
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Synonyms
CC-5013 hemihydrate
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Publications (64)
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Journal Impact Factor
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Most Recent
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Nature
2024 Sep;633(8030):670-677. PMID: 39198645 -
Cancer Cell
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 hemihydrate 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.
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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 hemihydrate 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.
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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 hemihydrate 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.
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Nat Chem Biol
2021 Jun;17(6):711-717. PMID: 34035522 -
Microbiome
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 -
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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
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
2025 Mar;39(3):720-733. PMID: 39885295 -
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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 hemihydrate 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.
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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
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]2019 Mar:125:392-402. PMID: 30660605 -
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bioRxiv
Regulation of BCL11A DNA binding and expression in human erythrocyte precursor HUDEP-2 cells. [Abstract]2026 Feb 8:2026.02.06.704516. PMID: 41822826 -
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Oxid Med Cell Longev
TNF- α Induces Neutrophil Apoptosis Delay and Promotes Intestinal Ischemia-Reperfusion-Induced Lung Injury through Activating JNK/FoxO3a Pathway. [Abstract]2021 Dec 29:2021:8302831. PMID: 35003520 -
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Elife
Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray syndrome. [Abstract]2018 Aug 1:7:e38430. PMID: 30067223
Lenalidomide hemihydrate 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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Lösungsmittel & Löslichkeit
In Vitro:
DMSO : 50 mg/mL (186.38 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : < 0.1 mg/mL (insoluble)
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- 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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (9.32 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.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (9.32 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.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%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
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protokoll
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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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.
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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.
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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.
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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
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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
Reinheit & Dokumentation
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Data Sheet (304 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
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- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
Verweise
[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]
Complete Stock Solution Preparation Table
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.7276 mL | 18.6379 mL | 37.2759 mL | 93.1897 mL |
| 5 mM | 0.7455 mL | 3.7276 mL | 7.4552 mL | 18.6379 mL | |
| 10 mM | 0.3728 mL | 1.8638 mL | 3.7276 mL | 9.3190 mL | |
| 15 mM | 0.2485 mL | 1.2425 mL | 2.4851 mL | 6.2126 mL | |
| 20 mM | 0.1864 mL | 0.9319 mL | 1.8638 mL | 4.6595 mL | |
| 25 mM | 0.1491 mL | 0.7455 mL | 1.4910 mL | 3.7276 mL | |
| 30 mM | 0.1243 mL | 0.6213 mL | 1.2425 mL | 3.1063 mL | |
| 40 mM | 0.0932 mL | 0.4659 mL | 0.9319 mL | 2.3297 mL | |
| 50 mM | 0.0746 mL | 0.3728 mL | 0.7455 mL | 1.8638 mL | |
| 60 mM | 0.0621 mL | 0.3106 mL | 0.6213 mL | 1.5532 mL | |
| 80 mM | 0.0466 mL | 0.2330 mL | 0.4659 mL | 1.1649 mL | |
| 100 mM | 0.0373 mL | 0.1864 mL | 0.3728 mL | 0.9319 mL |
Lenalidomide hemihydrate Related Classifications
HY-A0003B Related Classifications
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