Entrectinib (Rxdx-101)

N.º de catálogoS7998 Lote:S799803

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Datos técnicos

Fórmula

C31H34F2N6O2
Peso molecular 560.64 Número CAS 1108743-60-7
Solubilidad (25°C)* In vitro DMSO 100 mg/mL (178.36 mM)
Ethanol 75 mg/mL (133.77 mM)
Water Insoluble
In vivo (Agregue los solventes al producto individualmente y en orden.)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml significa ligeramente soluble o insoluble.
* Tenga en cuenta que Selleck prueba la solubilidad de todos los compuestos internamente, y la solubilidad real puede diferir ligeramente de los valores publicados. Esto es normal y se debe a ligeras variaciones entre lotes.
* Envío a temperatura ambiente (Las pruebas de estabilidad demuestran que este producto se puede enviar sin medidas de refrigeración.)

Preparación de soluciones madre

Actividad biológica

Descripción Entrectinib es un inhibidor pan-TrkA/B/C, ROS1 y ALK biodisponible por vía oral con un IC50 que oscila entre 0,1 y 1,7 nM. Entrectinib (RXDX-101) induce autophagy. Fase 2.
Objetivos
TrkA TrkB TrkC ROS1 ALK
In vitro

Entrectinib bloquea selectivamente la proliferación de líneas celulares dependientes de ALK e inhibe potentemente la señalización dependiente de ALK. Este compuesto también inhibe fuertemente el crecimiento celular de la línea celular de CPNM NCI-H2228 que presenta el reordenamiento EML4-ALK.

In vivo

En ratones portadores de xenoinjertos Karpas-299 y SR-786, Entrectinib (p.o.) induce la regresión tumoral completa. En ratones transgénicos NPM-ALK, este compuesto induce la regresión completa de las masas tumorales observadas en el timo y en los ganglios linfáticos.

En el modelo de xenoinjerto de NB, el cotratamiento con este compuesto mejoró la eficacia de la quimioterapia convencional.

Protocolo (de referencia)

Referencias

  • https://pubmed.ncbi.nlm.nih.gov/26457764/
  • http://mct.aacrjournals.org/content/8/12_Supplement/A244.short
  • http://cancerres.aacrjournals.org/content/75/15_Supplement/5390
  • https://pubmed.ncbi.nlm.nih.gov/36101520/
  • https://pubmed.ncbi.nlm.nih.gov/33229458/

Validación de productos por parte del cliente

Tumor cells were treated with entrectinib (10 nmol/L) for 4 hours or c-PARP for 48 hours, and harvested lysates were assessed by Western blotting. Data shown are representative of three independent experiments with similar results.

Datos de [ , , Clin Cancer Res, 2018, 24(10):2357-2369 ]

(A) We transfected the EGFP/Eluc gene into KM12SM cells to establish KM12SM/Eluc cells. KM12SM/Eluc cells were inoculated into the brain of SCID mice. The mice were treated daily with or without entrectinib (15 mg/kg) for 37 days until the bioluminescence increased. Mean ± SE of total flux are shown in the lower panel. Then, the entrectinib-treated brain tumor was harvested at the point indicated by the orange triangle and cultured in vitro. The expanded tumor cells were named KM12SM-ER. (B) The sensitivity of KM12SM-ER and KM12SM cells to entrectinib was determined through cell viability assays, using a CCK-8 kit. The data (mean ± standard deviation [SD] of triplicate cultures) shown are representative of three independent experiments with similar results. (C) Tumor cells were treated with entrectinib (10 nmol/L) for 4 h or c-PARP for 48 h, and harvested lysates were assessed by western blotting. Data shown are representative of three independent experiments with similar results.

Datos de [ , , Clin Cancer Res, 2018, doi: 10.1158/1078-0432.CCR-17-1623 ]

KM12C and KM12SM cells were treated with crizotinib (1 μmol/L) or entrectinib (1 μmol/L) for 2 h. Immunoblots of cell lysates from these treated cell lines are shown. The data are representative of three independent experiments, showing similar results.

Datos de [ , , Cancer Med, 2017, 6(12):2972-2983 ]

The effect of kinase inhibitors on signal transduction in human cancer cell lines in vitro. H1975 cells were treated with osimertinib (1 μmol/L) for 2 h. NUGC4 cells were treated with crizotinib (1 μmol/L) for 2 h, and then stimulated with HGF (50 ng/mL) for 10 min. KM12C and KM12SM cells were treated with crizotinib (1 μmol/L) or entrectinib (1 μmol/L) for 2 h. Immunoblots of cell lysates from these treated cell lines are shown.

Datos de [ , , Cancer Med, 2017, 6(12):2972-2983 ]

Sellecks Entrectinib (Rxdx-101) Ha sido citado por 61 Publicaciones

Targeting proteostasis in multiple myeloma through inhibition of LTK [ Leukemia, 2025, 10.1038/s41375-025-02682-8] PubMed: 40634511
Methylstat sensitizes ovarian cancer cells to PARP-inhibition by targeting the histone demethylases JMJD1B/C [ Cancer Gene Ther, 2025, 10.1038/s41417-025-00874-z] PubMed: 39915607
Zidesamtinib Selective Targeting of Diverse ROS1 Drug-Resistant Mutations [ Mol Cancer Ther, 2025, 10.1158/1535-7163.MCT-25-0025] PubMed: 40299789
Development of PROTACs for targeted degradation of oncogenic TRK fusions [ bioRxiv, 2025, 2025.06.18.660465] PubMed: 40666929
Clinical efficacy and identification of factors confer resistance to afatinib (tyrosine kinase inhibitor) in EGFR-overexpressing esophageal squamous cell carcinoma [ Signal Transduct Target Ther, 2024, 9(1):153] PubMed: 38937446
Pharmacological inhibition of PDGF-C/neuropilin-1 interaction: A novel strategy to reduce melanoma metastatic potential [ Biomed Pharmacother, 2024, 176:116766] PubMed: 38788599
Acquired NF2 mutation confers resistance to TRK inhibition in an ex vivo LMNA::NTRK1-rearranged soft-tissue sarcoma cell model [ J Pathol, 2024, 10.1002/path.6282] PubMed: 38613194
Acquired NF2 mutation confers resistance to TRK inhibition in an ex vivo LMNA::NTRK1-rearranged soft-tissue sarcoma cell model [ J Pathol, 2024, 263(2):257-269] PubMed: 38613194
LTK mutations responsible for resistance to lorlatinib in non-small cell lung cancer harboring CLIP1-LTK fusion [ Commun Biol, 2024, 7(1):412] PubMed: 38575808
Patient-derived rhabdomyosarcoma cells recapitulate the genetic and transcriptomic landscapes of primary tumors [ iScience, 2024, 27(10):110862] PubMed: 39319271

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