Linifanib (ABT-869) Property

Melting point:

180-183°C (dec.)

Boiling point:

542.2±50.0 °C(Predicted)

Density 

1.424

storage temp. 

-20°C Freezer

solubility 

DMSO, Methanol

form 

Brown powder.

pka

13.30±0.70(Predicted)

color 

Beige

Safety

HS Code 

2933998090

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Danger

Hazard statements

H361Suspected of damaging fertility or the unborn child

H372Causes damage to organs through prolonged or repeated exposure

H400Very toxic to aquatic life

H410Very toxic to aquatic life with long lasting effects

Precautionary statements

P201Obtain special instructions before use.

P202Do not handle until all safety precautions have been read and understood.

P260Do not breathe dust/fume/gas/mist/vapours/spray.

P264Wash hands thoroughly after handling.

P264Wash skin thouroughly after handling.

P270Do not eat, drink or smoke when using this product.

P273Avoid release to the environment.

P281Use personal protective equipment as required.

P308+P313IF exposed or concerned: Get medical advice/attention.

P314Get medical advice/attention if you feel unwell.

P391Collect spillage. Hazardous to the aquatic environment

P405Store locked up.

P501Dispose of contents/container to..…

Linifanib (ABT-869) Chemical Properties,Usage,Production

Chemical Properties

Beige Solid

Uses

Linifanib (ABT-869) is a novel, potent ATP-competitive RTK inhibitor for KDR, CSF-1R, Flt-1, Flt-3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM, 3 nM, and 66 nM respectively.

Uses

Linifanib (ABT 869) is an oral tyrosine kinase inhibitor with antineoplasic activity. As a dual inhibitor, Linifanib, is being tested on several different cancers.

Definition

ChEBI: A member of the class of ureas that is urea in which one of the nitrogens is substituted by a 2-fluoro-5-methylphenyl group, while the other nitrogen is substituted by a p-(3-amino-1H-indazol-4-yl)phenyl group. It is a poten , selective inhibitor of vascular endothelial growth factor and platelet-derived growth factor receptor tyrosine kinases.

Biological Activity

linifanib (abt-869) is an effective atp-competitive tyrosine kinase inhibitor against the platelet-derived growth factor (pdgf) receptor and the vascular endothelial growth factor receptor (vegfr) families, including constitutively active fms-like receptor tyrosine kinase 3 (flt3) [1][2]. it is of ic50 values of 0.55 nmol/l and 6 μmol/l to the cell growth in ba/f3 flt3 itd mutant cells and in ba/f3 flt3 wt cells, respectively [1].flt3 is important in controlling the proliferation and differentiation of hematopoietic cells. patients with acute myeloid leukemia (aml) showed activating mutations in flt3. these mutations caused abnormal cell proliferation [1].linifanib at a concentration of 10 nmol/l induced apoptosis in internal tandem duplication (itd) mutant cells, but showed no effect in wt cells. treatment with linifanib did not differentiate wt cells from flt3 mutant cells with mutation at d835v, in inhibiting proliferation or reducing cell viability. in ba/f3 flt3 itd cell lines, linifanib at a concentration of 10 nmol/l, effectively inhibited the phosphorylation of flt3. 10 nmol/l linifanib reduced the phosphorylation of akt at ser473 [1].daily orally treatment with linifanib by gavage in nod/scid mice with itd mutant cell decreased the leukemia progression rate compared with the control. on day 7, itd mutant cells showed rapid progression in control mice, whereas linifanib-treated mice showed no detectable disease. in addition, daily linifanib-treated mice with itd mutant cells showed significantly longer (p < 0.01) survival duration than control mice with itd mutant cells only [1].

target

VEGFR1/FLT1

storage

Store at -20°C

References

[1]. jenny e. hernandez-davies, joan p. zape, elliot m. landaw, et al. the multitargeted receptor tyrosine kinase inhibitor linifanib (abt-869) induces apoptosis through an akt and glycogen synthase kinase 3β–dependent pathway. mol. cancer ther., 2011, 10(6):949-59.
[2]. joyce e. ohm, michael r. shurin, clemens esche, et al. effect of vascular endothelial growth factor and flt3 ligand on dendritic cell generation in vivo. journal of immunology, 1999, 163:3260-3268.