TTNPB (Arotinoid Acid)

Catalog No.S4627 Synonyms: Ro 13-7410, AGN-191183

For research use only.

TTNPB (Arotinoid Acid, Ro 13-7410, AGN-191183) is a potent RAR agonist, and inhibits binding of [3H]tRA with IC50 of 5.1 nM, 4.5 nM, and 9.3 nM for human RARα, β, and γ, respectively.

TTNPB (Arotinoid Acid) Chemical Structure

CAS No. 71441-28-6

Selleck's TTNPB (Arotinoid Acid) has been cited by 8 Publications

Purity & Quality Control

Choose Selective Retinoid Receptor Inhibitors

Biological Activity

Description TTNPB (Arotinoid Acid, Ro 13-7410, AGN-191183) is a potent RAR agonist, and inhibits binding of [3H]tRA with IC50 of 5.1 nM, 4.5 nM, and 9.3 nM for human RARα, β, and γ, respectively.
RARβ [1]
(cell-free assay)
RARα [1]
(cell-free assay)
RARγ [1]
(cell-free assay)
4.5 nM 5.1 nM 9.3 nM
In vitro

TTNPB binds to nuclear retinoic acid receptors with high affinity, inhibits binding of [3H]tRA with IC50 of 3.8 nM, 4.0 nM, and 4.5 nM for mRARα, β, and γ, respectively. [1] TTNPB increases transcriptional activation of Mouse RARs in JEG-3 cells after 72 h using conditioned media with EC50 of 2.0 nM, 1.1 nM and 0.8 nM for mRARα, β, and γ, respectively. [2] TTNPB inhibits the growth of normal human mammary epithelial cells (HMECs) and estrogen receptor-positive (ER-positive) breast cancer cells by inducing G1 cell cycle blockade. [3] TTNPB causes a concentration-dependent decrease in ES-D3 cell differentiation. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HEK293 cells MXXGeY5kfGmxbjDhd5NigQ>? NHG1XI1C\2:waYP0JIFkfGm4aYT5JIF1KGi3bXHuJHJCWmGucHjhJIV5eHKnc4Pl[EBqdiCKRVuyPVMh[2WubIOgZpkhdHWlaX\ldoF{\SC{ZYDvdpRmeiCpZX7lJIF{e2G7LDDFR|UxRTBwMUigcm0> NWrG[XdGOjV|MEW2PFg>
CV-1 cells M4KyR2Z2dmO2aX;uJIF{e2G7 M3\HZWJqdmSrbnegZYZncW6rdImgZYdicW6|dDDy[ZRqdm:rYzDBZ4llKGejbX3hJJJm[2WydH;yd{Bkdy22cnHud4Zm[3SnZDDpcpRwKEOYLUGgZ4VtdHNuIFXDOVA:OC5yMEKg{rxu NInPR4k5OzB6OE[3
HL60 cells NWHDd|lHS3m2b4TvfIlkcXS7IHHzd4F6 NFXlWHhKdiC4aYTyc{BkgXSxdH;4bYNqfHliYXfhbY5{fCCKTE[wJINmdGy|LDDJR|UxRTR4IN88US=> MWWxNVEzQDZ2OB?=
HeLa cells MXPGeY5kfGmxbjDhd5NigQ>? Mn7ZRYdwdmm|dDDhZ5Rqfmm2eTDheEBpfW2jbjDSRXJidHCqYTDlfJBz\XO|ZXSgbY4hcHWvYX6gTIVN[SClZXzsd{Bie3Onc4Pl[EBieyC{ZXzheIl3\SCudX3pcoV{[2WwY3WgeY5qfHNiYYSgQl0yOCC3TTDifUBtfWOrZnXyZZNmKGG|c3H5JJJmdGG2aY\lJJRwKGOxboTyc4w> NV;MV2dCOTh7NUGwNlk>
In vivo TTNPB (0.25 mg/kg) causes growth inhibition in both MXT-HS and MXT-HI models by inducing cell apoptosis. [5]

Protocol (from reference)

Kinase Assay:[1]
  • Binding assays:

    Binding assays are performed as previously described (Allenby et al., 1993, 1994). Briefly, labeled and unlabeled retinoids are added to nucleosol or cytosolic fractions in ethanol so that the total amount of ethanol added is constant in all tubes and did not exceed 2% of the incubation volume. The receptor preparations are incubated with retinoids at 4°C for 4–6 hr. Sephadex PD-10 desalting columns are used to separate bound radioligand from free radioligand after equilib- rium is achieved. For competitive binding assays, varying concentrations of unlabeled competing ligand are incubated with the appropriate nucleosol or cytosol in the presence of a fixed concentration of [3H]tRA (sp. act. 49.3 Ci/mmol) or [3H]9-cis RA (sp. act. 24.0 Ci/mmol). Final concentrations of [3H] tRA and [3H]9-cis RA for nuclear receptor binding assays are 5nM. Final concentrations of [3H] tRA for CRABP binding assays is 30 nM. The IC50s are calculated as described above (DeLean et al., 1978). For saturation kinetics, increasing concentrations of radiolabeled ligand ([3H]tRA sp. act. 49.3 Ci/mmol, [3H]TTNPB sp. act. 5.5 Ci/ mmol) are added to the nucleosol of the appropriate receptor subtype in the presence (nonspecific binding) or absence (total binding) of a 100-fold molar excess of the corresponding unlabeled retinoid. Specific binding is defined as the total binding minus nonspecific binding. Saturation kinetics are calculated as previously described (Scatchard, 1949; Grippo and Gudas, 1987; Levin et al., 1992).

Cell Research:[3]
  • Cell lines: T47D cells and 184 cells
  • Concentrations: ~1 μM
  • Incubation Time: 8-12 days
  • Method: Human mammary epithelial cells are maintained in Mammary Epithelial Basal Medium (MEBM) supplemented with the Mammary Epithelial Growth Media (MEGM) bullet kit. 184 and 184B5 cells are maintained in MEBM sodium-bicarbonate free (MEBM-SBF) supplemented with the MEGM bullet kit, isoproterenol (10 μM), and transferrin (5 μg/ml). MCF10A cell lines are maintained in DME/F12 containing 5% heat inactivated horse serum, penicillin/streptomycin (100 μg/ml and 100 μg/ml), hydrocortisone (1.4μM), insulin (10 μg/ml), choleratoxin (100 ng/ml), and EGF (20 ng/ml). Breast cancer cell lines are maintained in Improved MEM Zinc Option containing 10% fetal bovine serum, 1% glutamine, and 1% penicillin/streptomycin. For growth assays, cells are treated with the different retinoids for the specified number of days with media and treatment changes every other day in T47D cells and every 2 days in 184 cells. Cell proliferation is measured according to the protocol for the CellTiter 96 Aqueous Non-Radioactive Cell Proliferation Assay. This colorimetric assay determines the number of viable cells in a sample. Each point represents samples done in quadruplicate.
Animal Research:[5]
  • Animal Models: Mouse models bearing hormone-sensitive (HS) and hormone-insensitive (HI) strains of the MXT murine mammary carcinoma.
  • Dosages: ~0.25 mg/kg
  • Administration: i.p.

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight 348.48


CAS No. 71441-28-6
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC(=CC1=CC=C(C=C1)C(=O)O)C2=CC3=C(C=C2)C(CCC3(C)C)(C)C

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