Lenalidomide hemihydrate (CC-5013 hemihydrate), a derivative of Thalidomide, acts as molecular glue. Lenalidomide hemihydrate is an orally active immunomodulator. Lenalidomide hemihydrate (CC-5013 hemihydrate) is a ligand of ubiquitin E3 ligase cereblon (CRBN), and it causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase. Lenalidomide hemihydrate (CC-5013 hemihydrate) specifically inhibits growth of mature B-cell lymphomas, including multiple myeloma, and induces IL-2 release from T cells[1][2].
IC50 & Target[5]
Cereblon
体外研究 (In Vitro)
Lenalidomide is potent in stimulating T cell proliferation and IFN-γ and IL-2 production. Lenalidomide has been shown to inhibit production of pro inflammatory cytokines TNF-α, IL-1, IL-6, IL-12 and elevate the production of anti-inflammatory cytokine IL-10 from human PBMCs. Lenalidomide downregulates the production of IL-6 directly and also by inhibiting multiple myeloma (MM) cells and bone marrow stromal cells (BMSC) interaction, which augments the apoptosis of myeloma cells[2]. Dose-dependent interaction with the CRBN-DDB1 complex is observed with Thalidomide, Lenalidomide and Pomalidomide, with IC50 values of ~30 μM, ~3 μM and ~3 μM, respectively, These reduced CRBN expression cells (U266-CRBN60 and U266-CRBN75) are less responsive than the parental cells to antiproliferative effects Lenalidomide across a dose-response range of 0.01 to 10 μM[3]. Lenalidomide, a thalidomide analog, functions as a molecular glue between the human E3 ubiquitin ligase cereblon and CKIα is shown to induce the ubiquitination and degradation of this kinase, thus presumably killing leukemic cells by p53 activation[5].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
The toxicity of Lenalidomide doses up to 15, 22.5, and 45 mg/kg via IV, IP, and PO routes of administration. Limited by solubility in our PBS dosing vehicle, these maximum achievable Lenalidomide doses are well tolerated with the exception of one mouse death (of four total dosed) at the 15 mg/kg IV dose. Notably, no other toxicities are observed in the study at IV doses of 15 mg/kg (n=3) or 10 mg/kg (n=45) or at any other dose level through IV, IP, and PO routes[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
268.27
Formula
C13H14N3O3.5
CAS 号
847871-99-2
中文名称
来那度胺半水合物；雷那度胺半水合物
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Omran A, et al. Effects of MRP8, LPS, and lenalidomide on the expressions of TNF-α , brain-enriched, and inflammation-related microRNAs in the primary astrocyte culture. ScientificWorldJournal. 2013 Sep 21;2013:208309.
[2]. Minzel W, et al. Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models. Cell. 2018 Sep 20;175(1):171-185.e25.
[3]. Kotla V, et al. Mechanism of action of lenalidomide in hematological malignancies. J Hematol Oncol. 2009 Aug 12;2:36.
[4]. Lopez-Girona A, et al. Cereblon is a direct protein target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide. Leukemia. 2012 Nov;26(11):2326-35.
[5]. Rozewski DM, et al. Pharmacokinetics and tissue disposition of lenalidomide in mice. AAPS J. 2012 Dec;14(4):872-82.
Cell Assay [3]
Cell lines NCI-H929 and U266, and DF15 cells are grown in RPMI-I640 medium containing 10% (V/V) heat-inactivated fetal bovine serum supplemented with 2 mM glutamine. To produce Lenalidomide resistant cell lines, NCI-H929 cells are treated continuously (fresh Lenalidomide is added every 3-4 days) with control (final 0.1% DMSO) or low-dose Lenalidomide (1 μM) for 2 months until the proliferation of cells is no longer inhibited by Lenalidomide (1 μM), as determined by cell viability (Vi-cell XR cell viability analyzer), cell proliferation by flow cytometry and cell cycle analysis (propidium iodide staining). After acquisition of resistance to 1 μM, the resistant H929 cell lines are treated with Lenalidomide (10 μM) for a further 4 months. After this period of time, the cell cultures achieved fully establish resistance up to high-dose Lenalidomide (30 μM). Prior to the experiments described here, H929 Lenalidomide-resistant cells are taken out of culture with compounds for 5-7 days before use[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [4]
Mice[4] Imprinting control region (ICR) mice 8-10 weeks of age are used. Lenalidomide is incompletely soluble at 3.5 mg/mL and above in PBS containing 1% HCl, as visible particulates remained after thorough mixing. Therefore 3 mg/mL is selected as the maximum dosing solution concentration (with no visible particulates). Single, individual mice are initially dosed with 3, 10, or 15 mg/kg IV; 4.5, 15, or 22.5 mg/kg IP; and 9, 30, or 45 mg/kg PO. Additional mice (n=4) are then evaluated at the maximum dose achievable by volume and solubility of Lenalidomide in the dosing solution. All mice are monitored closely for 1 h and re-evaluated for toxicities 3, 6, and 24 h postdose.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Omran A, et al. Effects of MRP8, LPS, and lenalidomide on the expressions of TNF-α , brain-enriched, and inflammation-related microRNAs in the primary astrocyte culture. ScientificWorldJournal. 2013 Sep 21;2013:208309.
[2]. Minzel W, et al. Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models. Cell. 2018 Sep 20;175(1):171-185.e25.
[3]. Kotla V, et al. Mechanism of action of lenalidomide in hematological malignancies. J Hematol Oncol. 2009 Aug 12;2:36.
[4]. Lopez-Girona A, et al. Cereblon is a direct protein target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide. Leukemia. 2012 Nov;26(11):2326-35.
[5]. Rozewski DM, et al. Pharmacokinetics and tissue disposition of lenalidomide in mice. AAPS J. 2012 Dec;14(4):872-82.
[1]. Monica M. Mita, et al. A phase Ia study of CC-90003, a selective extracellular signal-regulated kinase (ERK) inhibitor, in patients with relapsed or refractory BRAF or RAS-mutant tumors. Journal of Clinical Oncology 35, no. 15_suppl (May 20 2017) 2577-2577.
Pomalidomide-d3 (CC-4047-d3) is the deuterium labeled Pomalidomide. Pomalidomide, the third-generation immunomodulatory agent, acts as molecular glue. Pomalidomide interacts with the E3 ligase cereblon and induces degradation of essential Ikaros transcription factors[1][2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
276.26
Formula
C13H8D3N3O4
CAS 号
2093128-28-8
中文名称
泊马度胺 d3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Zhu YX, et al. Molecular mechanism of action of the immune-modulatory drugs, thalidomide, lenalidomide and pomalidomide in multiple myeloma. Leuk Lymphoma. 2013 Apr;54(4):683-7.
[3]. Hernandez-Ilizaliturri FJ1, et al. Immunomodulatory drug CC-5013 or CC-4047 and rituximab enhance antitumor activity in a severe combined immunodeficient mouse lymphoma model. Clin Cancer Res. 2005 Aug 15;11(16):5984-92.
[4]. Schafer PH, et al. Enhancement of cytokine production and AP-1 transcriptional activity in T cells by thalidomide-related immunomodulatory drugs. J Pharmacol Exp Ther. 2003 Jun;305(3):1222-32.
[5]. Li Z, et al. Pomalidomide shows significant therapeutic activity against CNS lymphoma with a major impact on the tumor microenvironment in murine models. PLoS One. 2013 Aug 5;8(8):e71754.
[6]. Lu J, et al. Hijacking the E3 Ubiquitin Ligase Cereblon to Efficiently Target BRD4. Chem Biol. 2015 Jun 18;22(6):755-63.
[7]. Liu D, et al. Tumour necrosis factor-α inhibits hepatic lipid deposition through GSK-3β/β-catenin signaling in juvenile turbot (Scophthalmus maximus L.). Gen Comp Endocrinol. 2016 Mar 1;228:1-8.
CC-115 hydrochloride is a potent and dual DNA-PK and mTOR kinase inhibitor with IC50s of 13 nM and 21 nM, respectively. CC-115 blocks both mTORC1 and mTORC2 signaling.
IC50 & Target[1]
DNA-PK
13 nM (IC50)
mTOR
21 nM (IC50)
mTORC1
mTORC2
PI3Kα
852 nM (IC50)
体外研究 (In Vitro)
CC-115 inhibits PC-3 cells proliferation with an IC50 of 138 nM. In a kinase selectivity assessment against a panel of 250 protein kinases at 3 μM, only one kinase other than mTOR kinase is identified with more than 50% inhibition (cFMS 57%, IC50=2.0 μM). Of the PI3K related kinases (PIKKs) tested, CC-115 proves to be equipotent against DNA PK (IC50=15 nM) and demonstrates 40 to >1000 fold selectivity against the remaining PIKKs tested; PI3K-alpha (IC50=0.85 μM), ATR (50% inhibition at 30 μM) and ATM (IC50>30 μM). The IC50 values for CC-115 are >10 μM against a panel of CYP enzymes and >33 μM for the hERG (human ether-a-go-go-related gene) ion channel. When screened in a single point assay at 10 μM against a Cerep receptor and enzyme panel only one target is inhibited >50% (PDE3, IC50=0.63 μM)[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
CC-115 hydrochloride shows good in vivo PK profiles across multiple species with 53%, 76% and ~100% oral bioavailability in mouse, rat and dog, respectively. CC-115 is tested at lower doses of 0.25, 0.5 and 1 mg/kg bid or 1 mg/kg qd, with observed corresponding tumor volume reductions of 46%, 57%, 66% and 57% respectively. CC-115 sustains inhibition though 24 hours. At the 1 mg/kg dose CC-115 shows significant inhibition at 1 and 3 hours, CC-115 demonstrating inhibition through 10 hours. CC-115 is evaluated using both once (qd) and twice (bid) daily dosing schedules[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
372.81
Formula
C16H17ClN8O
CAS 号
1300118-55-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Mortensen DS, et al. Optimization of a Series of Triazole Containing Mammalian Target of Rapamycin (mTOR) Kinase Inhibitors and the Discovery of CC-115. J Med Chem. 2015 Jul 23;58(14):5599-5608.
Kinase Assay [1]
An HTR-FRET substrate phosphorylation assay is employed for mTOR kinase. PI3Kα IC50 determinations are outsourced using the mobility shift assay format. Compounds (e.g., CC-115) are assessed against concentrations of ATP at approximately the Km for the assay, with average ATP Km of 15 μM and 50 μM for the mTOR and PI3K assays, respectively[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
PC-3 cells are cultured in growth media. For biomarker studies cells are treated for 1 h and then assayed for pS6 and pAkt levels using MesoScale technology. For proliferation experiments, cells are treated with compound (e.g., CC-115) and then allowed to grow for 72 h. All data are normalized and represented as a percentage of the DMSO-treated cells. Results are then expressed as IC50 values[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1]
Mice[1] Encouraged by the observed exposures, CC-115 is advanced into single dose PK/PD studies assessing mTOR pathway biomarker inhibition in tumor bearing mice. PC-3 tumor-bearing mice are administered with a single dose of CC-115, dosed orally at either 1 or 10 mg/kg, and plasma and tumor samples are collected at various time points for analysis. Significant inhibition of both mTORC1 (pS6) and mTORC2 (pAktS473) is observed for all compounds and the level of biomarker inhibition correlated to plasma compound levels.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Mortensen DS, et al. Optimization of a Series of Triazole Containing Mammalian Target of Rapamycin (mTOR) Kinase Inhibitors and the Discovery of CC-115. J Med Chem. 2015 Jul 23;58(14):5599-5608.
CC0651 is an allosteric inhibitor of the human Cdc34 ubiquitin-conjugating enzyme. CC0651 potently (IC50=1.72 μM) inhibits the ubiquitination of p27Kip1, as confirmed by dose-response analysis.
IC50 & Target
IC50: 1.72 μM (p27Kip1 ubiquitination)[1]
体外研究 (In Vitro)
CC0651 strongly impairs the rate of ubiquitin chain initiation on substrate by SCFCdc4, as measured by the monoubiquitination of Sic1 by K0 ubiquitin. CC0651 actually potentiates the formation of both ubiquitin dimers and monoubiquitinated hCdc34, concordant with the observed accumulation of the hCdc34 conjugate in cells treated with the ester derivative of CC0651. CC0651 completely inhibits the assembly of polyubiquitin chains and decreased formation of free triubiquitin and, to a lesser extent, hCdc34 monoubiquitin, but has no effect on production of diubiquitin[1]. CC0651 is an inhibitor of the E2 ubiquitin conjugating enzyme Cdc34A, acts by trapping a weak interaction between ubiquitin and the E2 donor ubiquitin binding site. A quantitative SCF ubiquitination assay with a β-Catenin substrate peptide yields a value of IC50 of 18±1 μM for CC0651 inhibition, similar to the effective concentrations observed in the NMR and TR-FRET assays[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
442.29
Formula
C20H21Cl2NO6
CAS 号
1319207-44-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Ceccarelli DF, et al. An allosteric inhibitor of the human Cdc34 ubiquitin-conjugating enzyme. Cell. 2011 Jun 24;145(7):1075-87.
[2]. Huang H, et al. E2 enzyme inhibition by stabilization of a low-affinity interface with ubiquitin. Nat Chem Biol. 2014 Feb;10(2):156-63.
Kinase Assay [1]
For small-molecule screens, p27Kip1 is ubiquitinated in a 15 μL reaction with 40 nM phospho-p27, 40 nM E1, 5 μM E2, 25 nM SCFSkp2, 25 nM Cks1, and 27.8 μM biotinylated ubiquitin in 40 mM Tris-HCl [pH 7.5], 5 mM MgCl2, 1 mM DTT, and 0.5 mM ATP at 23°C for 3 hr. The reaction is terminated with assay diluent, transferred to 384-well protein A plates coated with 62 ng SC528 antibody, incubated for 1 hr, and washed six times with 10 mM Tris-HCl [pH 7.6], 0.05% Tween20 prior to addition of 25 μL of 0.4 mg/mL europium streptavidin in HEPES [pH 7.6], 1% BSA, 0.2% Tween20 per well. Plates are incubated for 1 hr, washed, and read for Eu-time-resolved fluorescence after addition of 25 μL enhancement solution. For gel-based ubiquitination assays, CC0651 and its analogs are preincubated at the indicated concentrations with 0.5 μg E1, 1-4 μg hCdc34, and 50 ng SCFCdc4, 100 ng SCFFbw7, 150 ng SCFβTrCP, or 50 ng SCFSkp2 for 10-45 min at 4°C in 20 μL reaction buffer (50 mM HEPES [pH 7.5], 10 mM MgCl2, 2 mM ATP, and 50μM DTT). Reactions are initiated by addition of 1μg ubiquitin and respective SCF substrates (50 ng HisSic1 phosphorylated by Cln2-Cdc28, 50ng cyclin E phosphorylated by Cdk2, 25 ng biotinylated IκBα phosphopeptide [KKERLLDDHDpSGLDpSMKDEE], or 50 ng p27Kip1 phosphorylated by cyclin E-Cdk2), incubated at 30°C for 1-3 hr, and products visualized by immunoblot[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
PC-3 and HCT116 cell lines are grown in DMEM supplemented with Penicillin/Streptomycin, 2 mM glutamine, and 10% fetal bovine serum (FBS). Lentiviral shRNA constructs for human CDC34, UBE2R2, and nontarget control are used. For proliferation assays, PC-3 cultures are seeded at 5000 cells/well in quadruplicate in 24-well plates, grown for 24 hr, and then infected with lentiviral supernatant. For small-molecule inhibition, cells are seeded in quadruplicate at 500 cells/well in 96-well plates, grown for 24 hr, and treated with compound. Proliferation is measured by MTT assay. PC-3 or HCT 116 cultures are synchronized in G0/G1 by serum starvation for 30 hr and then released by addition of 10% serum. For epistasis experiments, PC-3 cells are infected with CDC34 shRNA for 24 hr, followed by addition of inhibitor and assessment of proliferation after 4 days. Anti-Cdc34, anti-p27, anti-α-tubulin, anti-ubiquitin, and anti-cyclin E antibodies are used[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Ceccarelli DF, et al. An allosteric inhibitor of the human Cdc34 ubiquitin-conjugating enzyme. Cell. 2011 Jun 24;145(7):1075-87.
[2]. Huang H, et al. E2 enzyme inhibition by stabilization of a low-affinity interface with ubiquitin. Nat Chem Biol. 2014 Feb;10(2):156-63.
CC260 is a selective PI5P4Kα and PI5P4Kβ inhibitor with Kis of 40 nM and 30 nM, respectively. CC260 does not inhibit or weakly inhibits other protein kinases, such as Plk1 and RSK2. CC260 can be used for cell energy metabolism, diabetes and cancer research[1].
IC50 & Target
Ki: 40 nM (PI5P4Kα) and 30 nM (PI5P4Kβ)[1]
体外研究 (In Vitro)
In cultured C2C12 myotubes, CC260 (20 μM) enhances Insulin-induced Akt phosphorylation at both Thr-308 and Ser-473 but suppresses S6K phosphorylation (Thr-389) by mTORC1[1]. CC260 (2.5 μM, 5 μM, 10 μM, 20 μM) significantly increases phosphorylation of acetyl-CoA carboxylase (ACC) in a dose-dependent manner[1]. CC260 treatment reduces the ability of BT474 cells to survive serum starvation, which could be rescued by expressing the PI5P4Kβ refractory mutant[1]. In BT474 cells, CC260 treatment causes an increase in glycolytic ATP production[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
490.43
Formula
C24H29Cl2N5O2
CAS 号
2411088-26-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Song Chen, et al. Pharmacological inhibition of PI5P4Kα/β disrupts cell energy metabolism and selectively kills p53-null tumor cells. Proc Natl Acad Sci U S A. 2021 May 25;118(21):e2002486118.
Rachelmycin (CC-1065; NSC 298223) 是一种从 Streptomyces zelensis 中分离得到有效的天然抗生素 (antibiotic)。Rachelmycin 在 B 型 DNA 的小沟中非共价和共价结合 (N-3 腺嘌呤加合物)。Rachelmycin 具有极强的抗肿瘤活性。
Rachelmycin Chemical Structure
CAS No. : 69866-21-3
规格
是否有货
5 mg
询价
10 mg
询价
25 mg
询价
* Please select Quantity before adding items.
生物活性
Rachelmycin (CC-1065; NSC 298223) is a potent naturally antibiotic isolated from Streptomyces zelensis. Rachelmycin binds non-covalently and covalently (N-3 adenine adduct) in the minor groove of B-form DNA. Rachelmycin has exceptionally potent antitumor activity[1].
体内研究 (In Vivo)
The smallest dose at which delayed death occurs is less for Rachelmycin (CC-1065; NSC 298223; 12.5 mg/kg) in experiments with non-tumored BDF1 mice[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
703.70
Formula
C37H33N7O8
CAS 号
69866-21-3
中文名称
拉奇霉素
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. W C Krueger, et al. Calf Thymus DNA binding/bonding Properties of CC-1065 and Analogs as Related to Their Biological Activities and Toxicities. Chem Biol Interact. 1992 Mar;82(1):31-46.
Rachelmycin (CC-1065; NSC 298223) 是一种从 Streptomyces zelensis 中分离得到有效的天然抗生素 (antibiotic)。Rachelmycin 在 B 型 DNA 的小沟中非共价和共价结合 (N-3 腺嘌呤加合物)。Rachelmycin 具有极强的抗肿瘤活性。
Rachelmycin Chemical Structure
CAS No. : 69866-21-3
规格
是否有货
5 mg
询价
10 mg
询价
25 mg
询价
* Please select Quantity before adding items.
生物活性
Rachelmycin (CC-1065; NSC 298223) is a potent naturally antibiotic isolated from Streptomyces zelensis. Rachelmycin binds non-covalently and covalently (N-3 adenine adduct) in the minor groove of B-form DNA. Rachelmycin has exceptionally potent antitumor activity[1].
体内研究 (In Vivo)
The smallest dose at which delayed death occurs is less for Rachelmycin (CC-1065; NSC 298223; 12.5 mg/kg) in experiments with non-tumored BDF1 mice[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
703.70
Formula
C37H33N7O8
CAS 号
69866-21-3
中文名称
拉奇霉素
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. W C Krueger, et al. Calf Thymus DNA binding/bonding Properties of CC-1065 and Analogs as Related to Their Biological Activities and Toxicities. Chem Biol Interact. 1992 Mar;82(1):31-46.
Rachelmycin (CC-1065; NSC 298223) 是一种从 Streptomyces zelensis 中分离得到有效的天然抗生素 (antibiotic)。Rachelmycin 在 B 型 DNA 的小沟中非共价和共价结合 (N-3 腺嘌呤加合物)。Rachelmycin 具有极强的抗肿瘤活性。
Rachelmycin Chemical Structure
CAS No. : 69866-21-3
规格
是否有货
5 mg
询价
10 mg
询价
25 mg
询价
* Please select Quantity before adding items.
生物活性
Rachelmycin (CC-1065; NSC 298223) is a potent naturally antibiotic isolated from Streptomyces zelensis. Rachelmycin binds non-covalently and covalently (N-3 adenine adduct) in the minor groove of B-form DNA. Rachelmycin has exceptionally potent antitumor activity[1].
体内研究 (In Vivo)
The smallest dose at which delayed death occurs is less for Rachelmycin (CC-1065; NSC 298223; 12.5 mg/kg) in experiments with non-tumored BDF1 mice[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
703.70
Formula
C37H33N7O8
CAS 号
69866-21-3
中文名称
拉奇霉素
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. W C Krueger, et al. Calf Thymus DNA binding/bonding Properties of CC-1065 and Analogs as Related to Their Biological Activities and Toxicities. Chem Biol Interact. 1992 Mar;82(1):31-46.
CC-99282 is a potent and orally active cereblon (CRBN) E3 ligase modulator (CELMoD). CC-99282 co-opts CRBN to induce potent and targeted degradation of Ikaros and Aiolos. CC-99282 can be used for researching non-Hodgkin lymphomas[1].
IC50 & Target[1]
Cereblon
分子量
535.57
Formula
C28H30FN5O5
CAS 号
2379572-34-4
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. J.-M. Michot, et al. A PHASE 1, MULTICENTER, OPEN-LABEL STUDY OF CC-99282 ALONE AND IN COMBINATION WITH RITUXIMAB IN PATIENTS WITH RELAPSED OR REFRACTORY NON-HODGKIN LYMPHOMAS. Hematological Oncology. Volume 39, Issue S2, Jun. 2021.
CC-17369 (7-Hydroxy pomalidomide) is a metabolite of Pomalidomide. CC-17369 is the Pomalidomide -based cereblon (CRBN) ligand used in the recruitment of CRBN protein. CC-17369 can be connected to the ligand for protein by a linker to form PROTAC[1].
IC50 & Target[2]
Cereblon
分子量
289.24
Formula
C13H11N3O5
CAS 号
1547162-46-8
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Hoffmann M, et al. Absorption, metabolism and excretion of [14C]pomalidomide in humans following oral administration. Cancer Chemother Pharmacol. 2013;71(2):489-501.
[2]. Makbul C, et al. Slowly folding surface extension in the prototypic avian hepatitis B virus capsid governs stability. Elife. 2020;9:e57277. Published 2020 Aug 14.
CC-17369 (7-Hydroxy pomalidomide) is a metabolite of Pomalidomide. CC-17369 is the Pomalidomide -based cereblon (CRBN) ligand used in the recruitment of CRBN protein. CC-17369 can be connected to the ligand for protein by a linker to form PROTAC[1].
IC50 & Target[2]
Cereblon
分子量
289.24
Formula
C13H11N3O5
CAS 号
1547162-46-8
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Hoffmann M, et al. Absorption, metabolism and excretion of [14C]pomalidomide in humans following oral administration. Cancer Chemother Pharmacol. 2013;71(2):489-501.
[2]. Makbul C, et al. Slowly folding surface extension in the prototypic avian hepatitis B virus capsid governs stability. Elife. 2020;9:e57277. Published 2020 Aug 14.
CC-17369 (7-Hydroxy pomalidomide) is a metabolite of Pomalidomide. CC-17369 is the Pomalidomide -based cereblon (CRBN) ligand used in the recruitment of CRBN protein. CC-17369 can be connected to the ligand for protein by a linker to form PROTAC[1].
IC50 & Target[2]
Cereblon
分子量
289.24
Formula
C13H11N3O5
CAS 号
1547162-46-8
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Hoffmann M, et al. Absorption, metabolism and excretion of [14C]pomalidomide in humans following oral administration. Cancer Chemother Pharmacol. 2013;71(2):489-501.
[2]. Makbul C, et al. Slowly folding surface extension in the prototypic avian hepatitis B virus capsid governs stability. Elife. 2020;9:e57277. Published 2020 Aug 14.
CC214-2 is a potent and dual inhibitor of mTORC1/mTORC2. Mycobacterium tuberculosis modulates mammalian target of rapamycin (mTOR) signaling to impede autophagy. CC214-2 has the potential to shorten the duration of TB[1].
分子量
383.44
Formula
C20H25N5O3
CAS 号
1228012-18-7
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Tasneen R, et al. Dual mTORC1/mTORC2 Inhibition as a Host-Directed Therapeutic Target in Pathologically Distinct Mouse Models of Tuberculosis. Antimicrob Agents Chemother. 2021;65(7):e0025321.
