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Cat. No. M6118
666-15 Structure
Size Price Availability Quantity
10mM*1mL In DMSO USD 177 In stock
5mg USD 130 In stock
10mg USD 220 In stock
50mg USD 830 In stock
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Quality Control
  • Current batch:
  • Purity >98%
  • COA
  • MSDS
Biological Activity

In vitro: 666-15 potently inhibits cancer cell growth. In MDA-MB-231 and MDA-MB-468 cells, the GI50 for 666-15 is 73 and 46 nM, respectively. In A549 and MCF-7 cells, it exhibits robust activity as well with GI50 of 0.47 and 0.31 μM. 666-15 is also found to be a rather weak inhibitor of CREB-CBP interaction with IC50 of 18.27 μM. 666-15 inhibits CREB’s transcription activity in living cells independent of direct CREB or CBP binding interaction. 666-15 is very potent in inhibiting CREB’s transcription activity. 666-15 also inhibits endogenous CREB target gene expression, the transcript level of nuclear receptor related 1 protein (Nurr1/NR4A2). In vivo: Preliminary toxicity studies show that intraperitoneal (ip) injection of 10 mg/kg of 666-15 is well tolerated in mice. The tumor growth in the mice treated with 666-15 is efficaciously inhibited with complete tumor stasis. During the same period, the tumor volume in the vehicle-treated group is more than tripled. The body weights of 666-15-treated animals and vehicle-treated ones are indistinguishable from each other during the entire treatment period.

Product Citations
Customer Product Validations & Biological Datas
Source Neurourol Urodyn. 2020 Apr. Figure 4. 666‐15 (Abmole Bioscience, Houston, TX, USA)
Method tested agonists and antagonists
Cell Lines HUCs
Concentrations 1×10^-9, 1×10^-8, 1×10^-7, 1×10^-6, and 1×10^-5 mol/L
Incubation Time 6h
Results Doses of 1×10^-9‐10^-6 mol/L for Formoterol, ICI 118551, BRL 37344, SR59230A, H89, and 666-15 did not significantly affect the viability of HUCs after 6hours.
Source Sci Rep (2016). Figure 2. 666-15
Method The luciferase activity assay
Cell Lines HEK 293T cells
Concentrations 5.0 μM
Incubation Time 5–7 h
Results Together with previous results of 666-15’s effect on other transcription factors22, these data demonstrate that 666-15 had little or no effect on MLL, c-Myb, YAP/TEAD or p53 driven transcription, and only affected NF-κB and SRF driven transcription at concentrations ~100 fold higher than those required for CREB driven transcription.
Cell Experiment
Cell lines MDA-MB-231 and MDA-MB-468 cells
Preparation method Cells are plated into 96-well plates and the cells are allowed to attach to the bottom of the plates overnight. Then the cells are treated with different concentrations of different drugs (666-15) for 72 h. The media are removed, and MTT reagent in complete tissue culture media is added to each well and incubated at 37 °C for 3 h. The incubation media are removed and 100 μL of DMSO is added to each well. The absorbance of the formed purple formazan solution is read at 570 nm using a plate reader.
Concentrations 80 nM
Incubation time 72 h.
Animal Experiment
Animal models BALB/c nude mouse
Formulation 1% N-methylpyrrolidone (NMP), 5% Tween-80 in water
Dosages 10 mg/kg
Administration i.v.
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Chemical Information
Molecular Weight 620.52
Formula C33H31Cl2N3O5
CAS Number 1433286-70-4
Purity >98%
Solubility 30 mg/mL in DMSO
Storage at -20°C

Design, synthesis and biological evaluation of regioisomers of 666-15 as inhibitors of CREB-mediated gene transcription.
Xie F, et al. Bioorg Med Chem Lett. 2017 Feb 15;27(4):994-998. PMID: 28073675.

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Keywords: 666-15 supplier, Epigenetic Reader Domain, inhibitors

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