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Fig. 1 · Structure
Cat. No.
A10679
CAS No.
728033-96-3
Formula
C22H16F3N3O2S
Mol. Weight
443.4

Documents & Downloads

OSI-930

Cat. No. A10679 CAS 728033-96-3

c-Kit/VEGFR Inhibitor

OSI-930 is a potent inhibitor of Kit, KDR, Flt, CSF-1R, c-Raf and Lck with IC50 of 80 nM, 9 nM, 8 nM, 15 nM, 41 nM and 22 nM, respectively.

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Biological Activity

Target & Activity

Target Activity Value
FLT1 IC50 8nM
KDR IC50 9nM
CSF-1R IC50 15nM
LCK IC50 22nM
C-Raf IC50 41nM
Kit IC50 80nM
FLT3 IC50 1.303μM
PDGFRα IC50 3.408μM
Abl IC50 4.738μM
PDGFRβ IC50 6.9μM
EGFR IC50 >10μM
AuroraA IC50 >10μM
Axl IC50 >10μM
CDK2/CyclinA IC50 >10μM
IKKβ IC50 >10μM
MEK1 IC50 >10μM
PDPK1 IC50 >10μM
PKBβ IC50 >10μM
Tie-2 IC50 >10μM

19 targets · Scroll to view more

In Vitro Studies

In MDA-MB-231 cells, OSI-930 at 1 μM significantly inhibited the PI3K/AKT pathway by reducing p-PI3K (Tyr458)/PI3K and p-AKT (Ser473)/AKT levels. In BT549 cells, OSI-930 at 1 μM significantly reduced p-AKT (Ser473)/AKT levels. In the absence of bacterial infection, 1μM OSI-930 alone did not significantly change EGR1 transcript levels in THP-1 cells compared with untreated control samples. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

PI3K/AKT pathway inhibition in MDA-MB-231 cells

Cell-based study · MDA-MB-231 cells [1]

In MDA-MB-231 cells, treatment at 1 μM significantly inhibited the PI3K/AKT pathway by reducing p-PI3K (Tyr458)/PI3K and p-AKT (Ser473)/AKT levels.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
p-AKT (Ser473)/AKTReported result significantly inhibited the PI3K/AKT pathway in MDA-MB-231 cells by reducing the levels of p-PI3K (Tyr458)/PI3K and p-AKT (Ser473)/AKT[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM
Reported limits
Not stated in the sentences used: route, schedule, vehicle, control.
Methods and source locations

Compound reported in the paper: OSI-930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > NCK synergizes with TKIs to stimulate intrinsic apoptosis (S137, S141)

p-AKT (Ser473)/AKT: p-AKT (Ser473)/AKT — Results > NCK synergizes with TKIs to stimulate intrinsic apoptosis (S141)

EGR1 transcript levels in uninfected THP-1 cells

Cell-based study · THP-1 cells [2]

In the absence of bacterial infection, treatment of THP-1 cells with 1μM OSI-930 alone did not significantly change EGR1 transcript levels compared with untreated control samples.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
EGR1 transcript levelsReported result 1μM OSI-930; in the absence of bacterial infection: treatment of THP-1 cells with OSI-930 alone did not significantly change EGR1 transcript levels.[2]

Literature-Reported Treatment Conditions

Treatment concentration
1μM
Reported limits
Not stated in the sentences used: route, schedule, vehicle.
Methods and source locations

Compound reported in the paper: OSI-930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Pathogenic Yersinia exploit host pathways regulated by the receptor tyrosine kinase c-KIT to suppress inflammatory cytokine release (S50); Figure 4 legend (S188, S190)

EGR1 transcript levels: EGR1 transcript levels; comparator: untreated THP1 control samples — Results > Pathogenic Yersinia exploit host pathways regulated by the receptor tyrosine kinase c-KIT to suppress inflammatory cytokine release (S50); Figure 4 legend (S188)

Reduced AKT phosphorylation in BT549 cells

Cell-based study · BT549 cells [1]

In BT549 cells, OSI-930 at 1 μM significantly reduced p-AKT (Ser473)/AKT levels.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
p-AKT (Ser473)/AKTReported result OSI-930 significantly reduced the level of p-AKT (Ser473)/AKT[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM
Reported limits
Not stated in the sentences used: route, schedule, vehicle, control.
Methods and source locations

Compound reported in the paper: OSI-930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > NCK synergizes with TKIs to stimulate intrinsic apoptosis (S137, S143)

p-AKT (Ser473)/AKT: p-AKT (Ser473)/AKT — Results > NCK synergizes with TKIs to stimulate intrinsic apoptosis (S143)

In Vivo Studies

Male C57BL/6 mice received OSI-930 intraperitoneally at 100 mg/kg body weight or vehicle. No hemorrhagic change was observed in the brain in either group. [3]

Brain hemorrhage assessment in mice

Animal study · Male C57BL/6 mice [3]

Male C57BL/6 mice received OSI-930 intraperitoneally at 100 mg/kg body weight or vehicle. No hemorrhagic change was observed in the brain in either group.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
the brain, no hemorrhagic changeReported result As for the brain, no hemorrhagic change was observed in control or OSI-930 groups.[3]

Conditions shared by the study groups

Route
intraperitoneally
Treatment course
daily for 1, 3, or 6 days; sacrificed 24 hours after the last injection
Vehicle
vehicle
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
OSI-930 100 mg/kg body weightvehicle was injectedAs for the brain, no hemorrhagic change was observed in control or OSI-930 groups.[3]
OSI-930 100 mg/kg body weight
Model: Male C57BL/6 mice
Methods and source locations

Compound reported in the paper: OSI-930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and methods > Animals (S6, S9, S10); Results > OSI-930 administration causes pituitary apoplexy (S39)

the brain, no hemorrhagic change: the brain, no hemorrhagic change; comparator: vehicle was injected — Results > OSI-930 administration causes pituitary apoplexy (S39)

OSI-930 100 mg/kg body weight · Materials and methods > Animals (S6, S10); Results > OSI-930 administration causes pituitary apoplexy (S39)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 728033-96-3
Applications c-Kit/VEGFR Inhibitor
Formula C22H16F3N3O2S
Molecular Weight 443.4
SMILES
C1=CC=C2C(=C1)C(=CC=N2)CNC3=C(SC=C3)C(=O)NC4=CC=C(C=C4)OC(F)(F)F

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 85 mg/mL (191.68 mM)
Water Insoluble
Ethanol 3 mg/mL

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
4 mg/mL
Vehicle
30% PEG400+0.5% Tween80+5% propylene glycol

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Tan YQ, Chiou YS, Guo H, et al. Vertical pathway inhibition of receptor tyrosine kinases and BAD with synergistic efficacy in triple negative breast cancer. NPJ Precis Oncol (2024). PMID: 38200104 DOI: 10.1038/s41698-023-00489-3 Source material
  2. [2] Micheva-Viteva SN, Shou Y, Nowak-Lovato KL, et al. c-KIT signaling is targeted by pathogenic Yersinia to suppress the host immune response. BMC Microbiol (2013). PMID: 24206648 DOI: 10.1186/1471-2180-13-249 Source material
  3. [3] Sugita Y, Takada S, Tanigaki K, et al. Inhibition of VEGF receptors induces pituitary apoplexy: An experimental study in mice. PLoS One (2023). PMID: 36928058 DOI: 10.1371/journal.pone.0279634 Source material

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