MedKoo Cat#: 100840 | Name: Thalidomide
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Description:

WARNING: This product is for research use only, not for human or veterinary use.

Thalidomide is a synthetic derivative of glutamic acid (alpha-phthalimido-glutarimide) with teratogenic, immunomodulatory, anti-inflammatory and anti-angiogenic properties. Thalidomide acts primarily by inhibiting both the production of tumor necrosis factor alpha (TNF-alpha) in stimulated peripheral monocytes and the activities of interleukins and interferons. This agent also inhibits polymorphonuclear chemotaxis and monocyte phagocytosis. In addition, thalidomide inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), thereby inhibiting angiogenesis.

Chemical Structure

Thalidomide
Thalidomide
CAS#50-35-1

Theoretical Analysis

MedKoo Cat#: 100840

Name: Thalidomide

CAS#: 50-35-1

Chemical Formula: C13H10N2O4

Exact Mass: 258.0641

Molecular Weight: 258.23

Elemental Analysis: C, 60.47; H, 3.90; N, 10.85; O, 24.78

Price and Availability

Size Price Availability Quantity
1g USD 90.00 Ready to ship
2g USD 150.00 Ready to ship
5g USD 250.00 Ready to ship
10g USD 450.00 Ready to ship
20g USD 750.00 Ready to ship
50g USD 1,450.00 Ready to ship
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Synonym
alphaphthalimidoglutarimide. Nphthaloylglutamimide; Nphthalylglutamic acid imide. US brand names: Synovir; Thalomid. Foreign brand names: Contergan; Distaval; Kevadon; Neurosedyn; Pantosediv; Sedoval K17; Softenon Talimol; Abbreviation: THAL.
IUPAC/Chemical Name
2-(2,6-dioxopiperidin-3-yl)isoindoline-1,3-dione
InChi Key
UEJJHQNACJXSKW-UHFFFAOYSA-N
InChi Code
InChI=1S/C13H10N2O4/c16-10-6-5-9(11(17)14-10)15-12(18)7-3-1-2-4-8(7)13(15)19/h1-4,9H,5-6H2,(H,14,16,17)
SMILES Code
O=C1N(C(CC2)C(NC2=O)=O)C(C3=C1C=CC=C3)=O
Appearance
Solid powder
Purity
>98% (or refer to the Certificate of Analysis)
Shipping Condition
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility
Soluble in DMSO, not in water
Shelf Life
>2 years if stored properly
Drug Formulation
This drug may be formulated in DMSO
Stock Solution Storage
0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code
2934.99.9001
More Info
Chemical structures: Chemical structures of Pomalidomide; Thalidomide and Lenalidomide are very similar:   Thalidomide is an off-white to white, odorless, crystalline powder that is soluble at 25°C in dimethyl sulfoxide and sparingly soluble in water and ethanol. The glutarimide moiety contains a single asymmetric center and, therefore, may exist in either of two optically active forms designated S-(-) or R-(+). THALOMID® (thalidomide) is an equal mixture of the S-(-) and R-(+) forms and, therefore, has a net optical rotation of zero. THALOMID® (thalidomide) is available in 50 mg, 100 mg, 150 mg and 200 mg capsules for oral administration. Active ingredient: thalidomide. Inactive ingredients: pregelatinized starch and magnesium stearate. The 50 mg capsule shell contains gelatin, titanium dioxide, and black ink. The 100 mg capsule shell contains black iron oxide, yellow iron oxide, titanium dioxide, gelatin, and black ink. The 150 mg capsule shell contains FD&C blue #2, black iron oxide, yellow iron oxide, titanium dioxide, gelatin, and black and white ink. The 200 mg capsule shell contains FD&C blue #2, titanium dioxide, gelatin, and white ink.   According to http://en.wikipedia.org/wiki/Thalidomide, Thalidomide was introduced as a sedative drug in the late 1950s. In 1961, it was withdrawn due to teratogenicity and neuropathy. There is now a growing clinical interest in thalidomide, and it is introduced as an immunomodulatory agent used primarily, combined with dexamethasone, to treat multiple myeloma. The drug is a potent teratogen in zebrafish, chickens, rabbits and primates including humans: severe birth defects may result if the drug is taken during pregnancy. Thalidomide was sold in a number of countries across the world from 1957 until 1961 when it was withdrawn from the market after being found to be a cause of birth defects in what has been called "one of the biggest medical tragedies of modern times".[4] It is not known exactly how many worldwide victims of the drug there have been, although estimates range from 10,000 to 20,000. Since then thalidomide has been found to be a valuable treatment for a number of medical conditions and it is being prescribed again in a number of countries, although its use remains controversial.  The thalidomide tragedy led to much stricter testing being required for drugs and pesticides before they can be licensed.   Thalidomide was developed by German pharmaceutical company Grünenthal in Stolberg (Rhineland) near Aachen, although this claim has recently been challenged. A report published by Martin W. Johnson, director of the Thalidomide Trust in the United Kingdom, mentioned evidence found by Argentinian author Carlos De Napoli that suggested the drug had been developed as an antidote to nerve gases such as Sarin in Germany in 1944, ten years before Grünenthal secured a patent in 1954. De Napoli suggested elsewhere that thalidomide may have been first synthesised by British scientists at the University of Nottingham in 1949. Thalidomide, launched by Grünenthal on 1st October 1957,  was found to act as an effective tranquiliser and painkiller and was proclaimed a "wonder drug" for insomnia, coughs, colds and headaches. It was also found to be an effective antiemetic which had an inhibitory effect on morning sickness, and so thousands of pregnant women took the drug to relieve their symptoms. At the time of the drug's development it was not thought likely that any drug could pass from the mother across the placental barrier and harm the developing fetus.     In 1964 Jacob Sheskin, Professor at the Hebrew University of Jerusalem at Hadassah University Hospital (he was also the chief staff and manager of Hansen Leper Hospital in Jerusalem), administered thalidomide to a critically ill patient with erythema nodosum leprosum (ENL), a painful complication of leprosy, in an attempt to relieve his pain in spite of the ban. The patient slept for hours, and was able to get out of bed without aid upon awakening. The result was followed by more favorable experiences and then by a clinical trial.[24] He found that patients with erythema nodosum leprosum, a painful skin condition, experienced relief of their pain by taking thalidomide. Further work conducted in 1991 by Dr. Gilla Kaplan at Rockefeller University in New York City showed that thalidomide worked in leprosy by inhibiting tumor necrosis factor alpha and believed it would be an effective treatment for AIDS. Kaplan partnered with Celgene Corporation to further develop the potential for thalidomide in AIDS and tuberculosis. However, clinical trials for AIDS proved disappointing. In 1964 Jacob Sheskin, Professor at the Hebrew University of Jerusalem at Hadassah University Hospital (he was also the chief staff and manager of Hansen Leper Hospital in Jerusalem), administered thalidomide to a critically ill patient with erythema nodosum leprosum (ENL), a painful complication of leprosy, in an attempt to relieve his pain in spite of the ban. The patient slept for hours, and was able to get out of bed without aid upon awakening. The result was followed by more favorable experiences and then by a clinical trial.[24] He found that patients with erythema nodosum leprosum, a painful skin condition, experienced relief of their pain by taking thalidomide. Further work conducted in 1991 by Dr. Gilla Kaplan at Rockefeller University in New York City showed that thalidomide worked in leprosy by inhibiting tumor necrosis factor alpha and believed it would be an effective treatment for AIDS. Kaplan partnered with Celgene Corporation to further develop the potential for thalidomide in AIDS and tuberculosis. However, clinical trials for AIDS proved disappointing. On July 16, 1998, the FDA approved the use of thalidomide for the treatment of lesions associated with Erythema Nodosum Leprosum (ENL). Because of thalidomideÂ’s potential for causing birth defects, the distribution of the drug was permitted only under tightly controlled conditions. The FDA required that Celgene Corporation, which planned to market thalidomide under the brand name Thalomid, establish a System for Thalidomide Education and Prescribing Safety (S.T.E.P.S.) oversight program. The conditions required under the program include; limiting prescription and dispensing rights only to authorized prescribers and pharmacies, keeping a registry of all patients prescribed thalidomide, providing extensive patient education about the risks associated with the drug and providing periodic pregnancy tests for women who are prescribed it.On May 26, 2006, the U.S. Food and Drug Administration granted accelerated approval for thalidomide (Thalomid, Celgene Corporation) in combination with dexamethasone for the treatment of newly diagnosed multiple myeloma (MM) patients.The FDA approval came seven years after the first reports of efficacy in the medical literature and Celgene took advantage of "off-label" marketing opportunities to promote the drug in advance of its FDA approval for the myeloma indication. Thalomid, as the drug is commercially known, sold over $300 million per year, while only approved for leprosy. From: http://en.wikipedia.org/wiki/Thalidomide    
Biological target:
Thalidomide-5-OH is the Thalidomide-based cereblon ligand used in the recruitment of CRBN protein.
In vitro activity:
Thalidomide upregulated five genes (AICDA, BMP, LEFTY1, LEFTY2, and TBX3) and downregulated one gene (ACTC1) (Table 1, Fig. 1B and C). The ratio of regulated genes, genes without change, and downregulated genes (5, 55, 1) was significantly different from the hypothetical ratio without change (0, 61, 0) (Fig. 1D, Fisher's exact test, P = 0.027). However, the ratio (5, 55, 1) was not significantly different from the hypothetical ratio with equal up- and downregulation (3, 55, 3) (Fig. 1D, Fisher's exact test, P = 0.581). These results suggest that although thalidomide affects undifferentiated hiPSCs, it might not facilitate or inhibit the undifferentiated state. Notably, three transforming growth factor β (TGF-β) genes (BMP2, LEFTY1, and LEFTY2), which are related to mesoderm differentiation, including limb formation, were upregulated (Fig. 1B). Reference: Biochem Biophys Rep. 2021 Mar 13;26:100978. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7973312/
In vivo activity:
The CRBN protein is involved in thalidomide-induced degradation of EGFL6. Overexpression of EGFL6 induced the development of abnormal subintestinal vein vessels in a zebrafish model, a process that was impaired by knocking down PAX6 or treatment with thalidomide. These findings established that thalidomide regulates EGFL6 expression through proteasome degradation to inhibit the EGFL6/PAX6 axis-driven angiogenesis in SBVM. Reference: Cell Mol Life Sci. 2020; 77(24): 5207–5221. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7671996/
Solvent mg/mL mM
Solubility
DMSO 33.0 127.79
DMSO:PBS (pH 7.2) (1:8) 0.1 0.43
DMF 12.0 46.47
Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 258.23 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
Formulation protocol:
1. Shimizu M, Tachikawa S, Saitoh N, Nakazono K, Yu-Jung L, Suga M, Ohnuma K. Thalidomide affects limb formation and multiple myeloma related genes in human induced pluripotent stem cells and their mesoderm differentiation. Biochem Biophys Rep. 2021 Mar 13;26:100978. doi: 10.1016/j.bbrep.2021.100978. PMID: 33763605; PMCID: PMC7973312. 2. Liao H, Li Y, Zhang X, Zhao X, Zheng D, Shen D, Li R. Protective Effects of Thalidomide on High-Glucose-Induced Podocyte Injury through In Vitro Modulation of Macrophage M1/M2 Differentiation. J Immunol Res. 2020 Aug 27;2020:8263598. doi: 10.1155/2020/8263598. PMID: 32908940; PMCID: PMC7474395. 3. Tang CT, Zhang QW, Wu S, Tang MY, Liang Q, Lin XL, Gao YJ, Ge ZZ. Thalidomide targets EGFL6 to inhibit EGFL6/PAX6 axis-driven angiogenesis in small bowel vascular malformation. Cell Mol Life Sci. 2020 Dec;77(24):5207-5221. doi: 10.1007/s00018-020-03465-3. Epub 2020 Feb 1. PMID: 32008086; PMCID: PMC7671996. 4. Chen LX, Ni XL, Zhang H, Wu M, Liu J, Xu S, Yang LL, Fu SZ, Wu J. Preparation, characterization, in vitro and in vivo anti-tumor effect of thalidomide nanoparticles on lung cancer. Int J Nanomedicine. 2018 Apr 23;13:2463-2476. doi: 10.2147/IJN.S159327. PMID: 29719394; PMCID: PMC5922239.
In vitro protocol:
1. Shimizu M, Tachikawa S, Saitoh N, Nakazono K, Yu-Jung L, Suga M, Ohnuma K. Thalidomide affects limb formation and multiple myeloma related genes in human induced pluripotent stem cells and their mesoderm differentiation. Biochem Biophys Rep. 2021 Mar 13;26:100978. doi: 10.1016/j.bbrep.2021.100978. PMID: 33763605; PMCID: PMC7973312. 2. Liao H, Li Y, Zhang X, Zhao X, Zheng D, Shen D, Li R. Protective Effects of Thalidomide on High-Glucose-Induced Podocyte Injury through In Vitro Modulation of Macrophage M1/M2 Differentiation. J Immunol Res. 2020 Aug 27;2020:8263598. doi: 10.1155/2020/8263598. PMID: 32908940; PMCID: PMC7474395.
In vivo protocol:
1. Tang CT, Zhang QW, Wu S, Tang MY, Liang Q, Lin XL, Gao YJ, Ge ZZ. Thalidomide targets EGFL6 to inhibit EGFL6/PAX6 axis-driven angiogenesis in small bowel vascular malformation. Cell Mol Life Sci. 2020 Dec;77(24):5207-5221. doi: 10.1007/s00018-020-03465-3. Epub 2020 Feb 1. PMID: 32008086; PMCID: PMC7671996. 2. Chen LX, Ni XL, Zhang H, Wu M, Liu J, Xu S, Yang LL, Fu SZ, Wu J. Preparation, characterization, in vitro and in vivo anti-tumor effect of thalidomide nanoparticles on lung cancer. Int J Nanomedicine. 2018 Apr 23;13:2463-2476. doi: 10.2147/IJN.S159327. PMID: 29719394; PMCID: PMC5922239.
  1: Jiang Y. Basic Science and Pathogenesis. Alzheimers Dement. 2024 Dec;20 Suppl 1:e090359. doi: 10.1002/alz.090359. PMID: 39751622. 2: Zavaleta-Monestel E, Quesada-Villaseñor R, Barrantes-López M, Arguedas-Chacón S, Campos-Hernández J, Rojas-Chinchilla C, García-Montero J, Castro-Ulloa J, Anchía-Alfaro A, Montenegro-Chaves JR. Advancements in the Treatment of Multiple Myeloma. Cureus. 2024 Dec 2;16(12):e74970. doi: 10.7759/cureus.74970. PMID: 39744254; PMCID: PMC11691229. 3: Heras Martinez HM, Barragan E, Marichev KO, Chávez-Flores D, Bugarin A. Phthalimides as anti-inflammatory agents. Future Med Chem. 2025 Jan;17(1):125-142. doi: 10.1080/17568919.2024.2437979. Epub 2024 Dec 17. PMID: 39740762. 4: Li R, Zeng Y, Chen Y, Ye Z, Chen C, Yang J, Fu J, Zhou T, Jiang D, Qin S, Ye H, Zhou Z, Zhang X. Cost-effectiveness analysis of combining lenalidomide with R-CHOP for treating diffuse large B-cell lymphoma in China. Front Pharmacol. 2024 Dec 16;15:1412743. doi: 10.3389/fphar.2024.1412743. PMID: 39737067; PMCID: PMC11682882. 5: Suresh B, Reshmi PR, Jaipal J, Pise GA, Prasad SS, Manohar N. Tofacitinib in Leprosy: A Novel Therapeutic Approach in Chronic Recalcitrant Type II Reactions. Cureus. 2024 Nov 28;16(11):e74694. doi: 10.7759/cureus.74694. PMID: 39735044; PMCID: PMC11681993. 6: Yang K, Lu Y, Gu J, Nie Y, Zhang T. Identifying novel aging-related diagnostic and prognostic models and aging-targeted drugs for sepsis patients. Sci Rep. 2024 Dec 28;14(1):31445. doi: 10.1038/s41598-024-83111-1. PMID: 39732977; PMCID: PMC11682178. 7: Liu S, Yuan F, Dong H, Zhang J, Mao X, Liu Y, Li H. PTGES3 proteolysis using the liposomal peptide-PROTAC approach. Biol Direct. 2024 Dec 26;19(1):144. doi: 10.1186/s13062-024-00580-0. PMID: 39726032; PMCID: PMC11670498. 8: Cai JF, Wei YR, Chen Y, Zou J, Yan S, Guan JL. A Triple Therapeutic Regiment Consisted of Colchicine, Thalidomide and Total Glucosides of Paeony Is Effective and Well-Tolerated for Treating Mucocutaneous Involvement in Patients With Behcet's Disease. Immun Inflamm Dis. 2024 Dec;12(12):e70057. doi: 10.1002/iid3.70057. PMID: 39722576; PMCID: PMC11669787. 9: Campione E, Cosio T, Pistoia ES, Artosi F, Shumack RG, Borselli C, Rivieccio A, Caputo V, Favaro M, Sorge R, Pica F, Bianchi L, Gaziano R. Prevalence of fungal colonization among patients with psoriasis in difficult-to-treat areas: impact of apremilast on mycotic burden and clinical outcomes. Front Immunol. 2024 Dec 10;15:1508489. doi: 10.3389/fimmu.2024.1508489. PMID: 39720714; PMCID: PMC11666449. 10: Sun X, Gong Y, Xie T, Fu Z, Lu D, Wei B, Cai Y, Yao W, Shen J. Nanoscale Liposomes Co-Loaded with Irinotecan Hydrochloride and Thalidomide for Colorectal Cancer Synergistic Therapy. Macromol Biosci. 2024 Dec 20:e2400478. doi: 10.1002/mabi.202400478. Epub ahead of print. PMID: 39704649. 11: Łacina P, Porzuczek D, Bogunia-Kubik K, Mazur G, Butrym A. Polymorphisms within genes encoding Ikaros family proteins IKZF1 and IKZF3 in multiple myeloma patients treated with thalidomide. Dent Med Probl. 2024 Nov-Dec;61(6):885-892. doi: 10.17219/dmp/183776. PMID: 39704419. 12: Deuitch NT, Schwartz DM, Aksentijevich I. Haploinsufficiency of A20. 2024 Dec 19. In: Adam MP, Feldman J, Mirzaa GM, Pagon RA, Wallace SE, Amemiya A, editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993–2024. PMID: 39715316. 13: De Santis M, Tonutti A, Isailovic N, Motta F, Rivara RM, Ragusa R, Guidelli GM, Caprioli M, Ceribelli A, Renna D, Luciano N, Selmi C. Serum IL-23 levels reflect a myeloid inflammatory signature and predict the response to apremilast in patients with psoriatic arthritis. Front Immunol. 2024 Dec 4;15:1455134. doi: 10.3389/fimmu.2024.1455134. PMID: 39697337; PMCID: PMC11652657. 14: Bergantim R, Geraldes C, João C, Lúcio P, Neves M, Trigo F, Pedrosa H, Ventura M, Santos S, Ramos D. The evolving treatment landscape of multiple myeloma in Portugal: A nation-wide retrospective cohort study of real-world clinical practice. EJHaem. 2024 Oct 28;5(6):1144-1153. doi: 10.1002/jha2.1035. PMID: 39691257; PMCID: PMC11647699. 15: Neema S, Vendhan S, Shah N, Kashif AW, Vasudevan B. Successful Management of Epidermolysis Bullosa Pruriginosa with Oral Thalidomide: A Case Report of Rare Dystrophic EB Subset. Indian J Dermatol. 2024 Nov-Dec;69(6):483-485. doi: 10.4103/ijd.ijd_269_24. Epub 2024 Oct 29. PMID: 39678751; PMCID: PMC11642455. 16: Awasthi S, Nijhawan M, Mishra A, Gupta A. Comparing the efficacy of oral apremilast, intralesional corticosteroids, and their combination in patients with patchy alopecia areata: a randomized clinical controlled trial. Arch Dermatol Res. 2024 Dec 14;317(1):129. doi: 10.1007/s00403-024-03642-5. PMID: 39673617. 17: Yang K, Gong Y, Xiao J. Evaluating the Role of Red Blood Cell Lifespan in Transfusion-Dependent β-Thalassemia and Impact of Thalidomide Treatment. Am J Hematol. 2024 Dec 9. doi: 10.1002/ajh.27557. Epub ahead of print. PMID: 39651701. 18: Gardner JA, Sprague J, Greipp PT, Conant JL. B-Lymphoblastic Leukemia with BCR::ABL1-like Features After Long-term Lenalidomide Therapy. J Assoc Genet Technol. 2024;50(4):188-192. PMID: 39645610. 19: Motamed-Sanaye A, Mortezaei A, Afshari AR, Saadatian Z, Faraji AH, Sheehan JP, Mokhtari AM. Angiogenesis inhibitors effects on overall survival and progression-free survival in newly diagnosed primary glioblastoma multiforme: a meta-analysis of twelve randomized clinical trials. J Neurooncol. 2025 Jan;171(2):313-328. doi: 10.1007/s11060-024-04865-2. Epub 2024 Dec 5. PMID: 39636552. 20: Yang WJ, Shi LD, Liang Y, Liang LM, Zhang H, Wang L, Zhou Q. Comparison of Efficacy and Safety Outcomes of Different Doses Schedules of Thalidomide for Treating Moderate-to-Severe β-Thalassemia Patients. Ther Clin Risk Manag. 2024 Nov 29;20:799-809. doi: 10.2147/TCRM.S481128. PMID: 39633983; PMCID: PMC11616116.