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Dokumenty

SML3055

Sigma-Aldrich

LY3009120

≥98% (HPLC)

Synonim(y):

1-(3,3-Dimethylbutyl)-3-(2-fluoro-4-methyl-5-(7-methyl-2-(methylamino)pyrido[2,3-d]pyrimidin-6-yl)phenyl)urea, DP 4978, DP-4978, DP4978, LY 3009120, LY-3009120, N-(3,3-Dimethylbutyl)-N′-[2-fluoro-4-methyl-5-[7-methyl-2-(methylamino)pyrido[2,3-d]pyrimidin-6-yl]phenyl]urea

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About This Item

Wzór empiryczny (zapis Hilla):
C23H29FN6O
Numer CAS:
1454682-72-4
Masa cząsteczkowa:
424.51
Numer MDL:
MFCD28411374
Kod UNSPSC:
12352200
NACRES:
NA.77

Poziom jakości

100

Próba

≥98% (HPLC)

Postać

powder

kolor

white to beige

rozpuszczalność

DMSO: 2 mg/mL, clear (warmed)

temp. przechowywania

2-8°C

ciąg SMILES

CC1=CC(F)=C(C=C1C2=C(N=C3N=C(N=CC3=C2)NC)C)NC(NCCC(C)(C)C)=O

InChI

1S/C23H29FN6O/c1-13-9-18(24)19(29-22(31)26-8-7-23(3,4)5)11-16(13)17-10-15-12-27-21(25-6)30-20(15)28-14(17)2/h9-12H,7-8H2,1-6H3,(H2,26,29,31)(H,25,27,28,30)

Klucz InChI

HHCBMISMPSAZBF-UHFFFAOYSA-N

Działania biochem./fizjol.

LY3009120 is an orally active, potent and selective pan-RAF type II inhibitor (IC50 = 4.3 nM/CRAF (c-Raf, Raf-1), 5.8 nM/BRAF(V600E), 15 nM/BRAF (b-Raf) by kinase assay with 1 mM ATP; IC50 = 44 nM/ARAF, 31-47 nM/BRAF, 42 nM/CRAF, >1 μM/155 other kinases by cell-based KiNativ affinity binding assay). LY3009120 inhibits RAF-dependent proliferation in cancer cultures (A375/HCT116 IC50 = 9.2/220 nM) and exhibits anti-tumor efficacy in a rat BRAF V600E ST019VR PDX model in vivo (15-30 mg/kg b.i.d. p.o.).
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Kod klasy składowania

11 - Combustible Solids

Klasa zagrożenia wodnego (WGK)

WGK 3

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable

Certyfikaty analizy (CoA)

Poszukaj Certyfikaty analizy (CoA), wpisując numer partii/serii produktów. Numery serii i partii można znaleźć na etykiecie produktu po słowach „seria” lub „partia”.

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

S-H Chen et al.
Oncogene, 37(6), 821-832 (2017-10-24)
KRAS, NRAS and BRAF mutations are among the most important oncogenic drivers in many major cancer types, such as melanoma, lung, colorectal and pancreatic cancer. There is currently no effective therapy for the treatment of RAS mutant cancers. LY3009120, a
Sheng-Bin Peng et al.
Cancer cell, 28(3), 384-398 (2015-09-08)
LY3009120 is a pan-RAF and RAF dimer inhibitor that inhibits all RAF isoforms and occupies both protomers in RAF dimers. Biochemical and cellular analyses revealed that LY3009120 inhibits ARAF, BRAF, and CRAF isoforms with similar affinity, while vemurafenib or dabrafenib
Shih-Hsun Chen et al.
Cancer discovery, 6(3), 300-315 (2016-01-07)
We have identified previously undiscovered BRAF in-frame deletions near the αC-helix region of the kinase domain in pancreatic, lung, ovarian, and thyroid cancers. These deletions are mutually exclusive with KRAS mutations and occur in 4.21% of KRAS wild-type pancreatic cancer.
Wei-Jun Wei et al.
Theranostics, 7(4), 987-1001 (2017-04-07)
Although the prognosis of differentiated thyroid cancer (DTC) is relatively good, 30-40% of patients with distant metastases develop resistance to radioactive iodine therapy due to tumor dedifferentiation. For DTC patients harboring BRAFV600E mutation, Vemurafenib, a BRAF kinase inhibitor, has dramatically
James R Henry et al.
Journal of medicinal chemistry, 58(10), 4165-4179 (2015-05-13)
The RAS-RAF-MEK-MAPK cascade is an essential signaling pathway, with activation typically mediated through cell surface receptors. The kinase inhibitors vemurafenib and dabrafenib, which target oncogenic BRAF V600E, have shown significant clinical efficacy in melanoma patients harboring this mutation. Because of
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