CUDC-101

Catalog No.S1194

For research use only.

CUDC-101 is a potent multi-targeted inhibitor against HDAC, EGFR and HER2 with IC50 of 4.4 nM, 2.4 nM, and 15.7 nM, and inhibits class I/II HDACs, but not class III, Sir-type HDACs. Phase 1.

CUDC-101 Chemical Structure

CAS No. 1012054-59-9

Selleck's CUDC-101 has been cited by 17 publications

Purity & Quality Control

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Biological Activity

Description CUDC-101 is a potent multi-targeted inhibitor against HDAC, EGFR and HER2 with IC50 of 4.4 nM, 2.4 nM, and 15.7 nM, and inhibits class I/II HDACs, but not class III, Sir-type HDACs. Phase 1.
Targets
EGFR [1]
(Cell-free assay)
HDAC [1]
(Cell-free assay)
HDAC1 [1]
(Cell-free assay)
HDAC6 [1]
(Cell-free assay)
HDAC3 [1]
(Cell-free assay)
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2.4 nM 4.4 nM 4.5 nM 5.1 nM 9.1 nM
In vitro

Specific for class I and class II HDACs, CUDC-101 does not inhibit class III Sir-type HDACs. CUDC-101 displays weak activity against other protein kinases including KDR/VEGFR2, Lyn, Lck, Abl-1, FGFR-2, Flt-3, and Ret with IC50 of 0.85 μM, 0.84 μM, 5.91 μM, 2.89 μM, 3.43 μM, 1.5 μM, abd 3.2 μM, respectively. CUDC-101 displays broad antiproliferative activity in many human cancer cell types with IC50 of 0.04-0.80 μM, exhibiting a higher potency than erlotinib, lapatinib, and combinations of vorinostat with either erlotinib or lapatinib in most cases. CUDC-101 potently inhibits lapatinib- and erlotinib-resistant cancer cell lines. [1] CUDC-101 inhibits the erlotinib-resistant EGFR mutant T790M although its effects are incomplete with an Amax of ~60% of peak enzyme activity after inhibition. CUDC-101 treatment increases the acetylation of histone H3 and H4, as well as the acetylation of non-histone substrates of HDAC such as p53 and α-tubulin, in a dose-dependant manner in various cancer cell lines. CUDC-101 also suppresses HER3 expression, Met amplification, and AKT reactivation in tumor cells. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human SK-BR-3 cells M4rx[3Bzd2yrZnXyZZRqd25iYYPzZZk> MWjBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFONLVLSMVMh[2WubIOgZYZ1\XJiaILzJIJ6KEGWUDDjc451\W62IHHzd4F6NCCLQ{WwQVAvODRizszN MmnVNlAyPDN5N{i=
MDA-MB-231 cells M33NUXBzd2yrZnXyZZRqd25iYYPzZZk> MlvXRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPRFGtUWIuOjNzIHPlcIx{KGGodHXyJIhzeyCkeTDBWHAh[2:wdHXueEBie3OjeTygTWM2OD1yLkGg{txO MVKyNFE1Ozd5OB?=
human HepG2 cells Mn72VJJwdGmoZYLheIlwdiCjc4PhfS=> NID6dGNCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjldGczKGOnbHzzJIFnfGW{IHjyd{BjgSCDVGCgZ49vfGWwdDDhd5NigSxiSVO1NF0xNjF|IN88US=> NIXYcmgzODF2M{e3PC=>
human SKHEP1 cells NGrWNIFRem:uaX\ldoF1cW:wIHHzd4F6 MkKyRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCVS1jFVFEh[2WubIOgZYZ1\XJiaILzJIJ6KEGWUDDjc451\W62IHHzd4F6NCCLQ{WwQVAvOjJizszN MV[yNFE1Ozd5OB?=
human Hep3B2 cells M2HTZXBzd2yrZnXyZZRqd25iYYPzZZk> NUTzVJB5SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDI[ZA{SjJiY3XscJMh[W[2ZYKgbJJ{KGK7IFHUVEBkd262ZX70JIF{e2G7LDDJR|UxRTBwMkOg{txO MViyNFE1Ozd5OB?=
human BxPC3 cells MUfQdo9tcW[ncnH0bY9vKGG|c3H5 M2DVWWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iQojQR|Mh[2WubIOgZYZ1\XJiaILzJIJ6KEGWUDDjc451\W62IHHzd4F6NCCLQ{WwQVAvOjdizszN M1TXWVIxOTR|N{e4
human NCI-H358 cells NVXWdoR4WHKxbHnm[ZJifGmxbjDhd5NigQ>? M2LLdmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg{PThiY3XscJMh[W[2ZYKgbJJ{KGK7IFHUVEBkd262ZX70JIF{e2G7LDDJR|UxRTBwNDFOwG0> M{fDdVIxOTR|N{e4
human MCF7 cells M1f3PXBzd2yrZnXyZZRqd25iYYPzZZk> MlL5RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPQ1[3JINmdGy|IHHmeIVzKGi{czDifUBCXFBiY3;ueIVvfCCjc4PhfUwhUUN3ME2wMlU2KM7:TR?= NVjpbHhYOjBzNEO3O|g>
human HCC827 cells M4HJTXBzd2yrZnXyZZRqd25iYYPzZZk> MVvBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiFQ{iyO{Bk\WyuczDh[pRmeiCqcoOgZpkhSVSSIHPvcpRmdnRiYYPzZZktKEmFNUC9NE43KM7:TR?= NGji[2kzODF2M{e3PC=>
human H460 cells MlnkVJJwdGmoZYLheIlwdiCjc4PhfS=> MUXBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEh2NkCgZ4VtdHNiYX\0[ZIhcHK|IHL5JGFVWCClb370[Y51KGG|c3H5MEBKSzVyPUCuO{DPxE1? NWfDXI1zOjBzNEO3O|g>
human Capan1 cells NISzUFBRem:uaX\ldoF1cW:wIHHzd4F6 M2LmSGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iQ3HwZY4yKGOnbHzzJIFnfGW{IHjyd{BjgSCDVGCgZ49vfGWwdDDhd5NigSxiSVO1NF0xNjhizszN M{\FVFIxOTR|N{e4
In vivo Administration of CUDC-101 at 120 mg/kg/day induces tumor regression in the Hep-G2 liver cancer model, which is more efficacious than that of erlotinib at its maximum tolerated dose (25 mg/kg/day) and vorinostat at an equimolar concentration dose (72 mg/kg/day). CUDC-101 inhibits the growth of erlotinib-sensitive H358 NSCLC xenografts in a dose-dependent manner. CUDC-101 also shows potent inhibition of tumor growth in the erlotinib-resistant A549 NSCLC xenograft model. CUDC-101 produces significant tumor regression in the lapatinib-resistant, HER2-negative, EGFR-overexpressing MDA-MB-468 breast cancer model and the EGFR-overexpressing CAL-27 head and neck squamous cell carcinoma (HNSCC) model. Additionally, CUDC-101 inhibits tumor growth in the K-ras mutant HCT116 colorectal and EGFR/HER2 (neu)-expressing HPAC pancreatic cancer models. [1]

Protocol (from reference)

Kinase Assay:[1]
  • HDAC, EGFR and HER2 inhibition assays:

    The activities of Class I and II HDACs are assessed using the Biomol Color de Lys system. Briefly, HeLa cell nuclear extracts are used as a source of HDACs. Different concentrations of CUDC-101 are added to HeLa cell nuclear extracts in the presence of a colorimetric artificial substrate. Developer is added at the end of the assay and enzyme activity is measured in the Wallac Victor II 1420 microplate reader at 405 nM. EGFR and HER2 kinase activity are measured using HTScan EGF receptor and HER2 kinase assay kits. Briefly, the GST-EGFR fusion protein is incubated with synthetic biotinylated peptide substrate and varying concentrations of CUDC-101 in the presence of 400 mM ATP. Phosphorylated substrate is captured with strapavidin-coated 96-well plates. The level of phosphorylation is monitored by antiphospho-tyrosine- and europium-labeled secondary antibodies. The enhancement solution is added at the end of the assay and enzyme activity is measured in the Wallac Victor II 1420 microplate reader at 615 nM.

Cell Research:[1]
  • Cell lines: HCC827, H358, H460, HepG2, Hep3B2, Sk-Hep-1, Capan1, BxPc3, MCF-7, MDA-MB-231, and Sk-Br-3
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 72 hours
  • Method: Cancer cell lines are plated at 5000 to 10000 cells per well in 96-well flatbottomed plates with varying concentrations of CUDC-101. The cells are incubated with CUDC-101 for 72 hours in the presence of 0.5% of fetal bovine serum. Growth inhibition is assessed by an adenosine triphosphate (ATP) content assay using the Perkin-Elmer ATPlite kit. Apoptosis is routinely assessed by measuring the activities of Caspase-3 and -7 using Apo-ONE Homogeneous Assay Kit.
Animal Research:[1]
  • Animal Models: Female athymic mice (nude nu/nu CD-1) inoculated with Hep-G2, H358, A549, MDA-MB468, HCT116, CAL-27, HepG2, or HPAC
  • Dosages: ~120 mg/kg/day
  • Administration: Administered via i.v.

Solubility (25°C)

In vitro

In vivo

Add solvents to the product individually and in order
(Data is from Selleck tests instead of citations):
15% Captisol
For best results, use promptly after mixing.

30 mg/mL

Chemical Information

Molecular Weight 434.49
Formula

C24H26N4O4

CAS No. 1012054-59-9
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles COC1=C(C=C2C(=C1)N=CN=C2NC3=CC=CC(=C3)C#C)OCCCCCCC(=O)NO

In vivo Formulation Calculator (Clear solution)

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Molarity Calculator

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Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT01702285 Terminated Drug: CUDC-101 Cancer Curis Inc. September 2012 Phase 1
NCT01384799 Completed Drug: CUDC-101|Drug: Cisplatin|Radiation: Radiation Therapy Head and Neck Cancer Curis Inc. November 2011 Phase 1
NCT00728793 Completed Drug: CUDC-101 Tumors Curis Inc. August 2008 Phase 1

(data from https://clinicaltrials.gov, updated on 2022-08-01)

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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