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Entrectinib-d8

CAT: 0804-HY-12678S1-01Size: 1 mgDry Ice: NoHazardous: No
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CAT#:0804-HY-12678S1-01Size:1 mg
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24/48H Stock Items & 2 to 6 Weeks non Stock Items.
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Description
Entrectinib-d8 (NMS-E628-d8; RXDX-101-d8) is a deuterated version of Entrectinib. Entrectinib (NMS-E628) is an orally available, blood-brain barrier permeable, central nervous system active TrkA/B/C, ROS1 and ALK inhibitor with IC50 values of 1, 3, 5, 12 and 12, respectively. 7 nM. Entrectinib induces apoptosis and cycle arrest in cancer cells, has anti-tumor activity, and also alleviates bleomycin-induced pulmonary fibrosis in mice[1][2][3][4].
CAS Number
2251773-94-9
Product Name Alternative
NMS-E628-d8; RXDX-101-d8
UNSPSC
12352005
Target
Anaplastic lymphoma kinase (ALK) ; Autophagy; Isotope-Labeled Compounds; ROS Kinase; Trk Receptor
Type
Isotope-Labeled Compounds
Related Pathways
Autophagy; Neuronal Signaling; Others; Protein Tyrosine Kinase/RTK
Applications
Cancer-Kinase/protease
Field of Research
Cancer
Purity
99.82
Solubility
DMSO : 100 mg/mL (ultrasonic)
Smiles
O=C(NC1=NNC2=C1C=C(CC3=CC(F)=CC(F)=C3)C=C2)C4=C(NC5CCOCC5)C=C(N6C([2H])([2H])C([2H])([2H])N(C)C([2H])([2H])C6([2H])[2H])C=C4
Molecular Formula
C31H26D8F2N6O2
Molecular Weight
568.69
References & Citations
[1]Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53 (2) :211-216.|[2]Miao Y, et al. Entrectinib ameliorates bleomycin-induced pulmonary fibrosis in mice by inhibiting TGF-β1 signaling pathway. Int Immunopharmacol. 2022 Dec;113 (Pt B) :109427. |[3]Ardini E, et al. Entrectinib, a Pan-TRK, ROS1, and ALK Inhibitor with Activity in Multiple Molecularly Defined Cancer Indications. Mol Cancer Ther. 2016 Apr;15 (4) :628-39.|[4]Iyer R, et al. Entrectinib is a potent inhibitor of Trk-driven neuroblastomas in a xenograft mouse model. Cancer Lett. 2016 Mar 28;372 (2) :179-86.
Shipping Conditions
Room Temperature
Storage Conditions
-20°C, 3 years; 4°C, 2 years (Powder)
Scientific Category
Isotope-Labeled Compounds
Clinical Information
No Development Reported

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