| Field | Specification |
|---|---|
| Target | |
| Alternative names | Q702 TFA |
| Applications | |
| Molecular weight | |
| Molecular formula | C27H25F6N5O7 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Adrixetinib TFA, also known as Q702 TFA, is an orally active triple inhibitor of CSF1R, Mer, and Axl, with Kd values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. It acts as an immune modulator that remodels the tumor microenvironment, increasing M1 macrophages and CD8+ T cells while reducing M2 macrophages and myeloid-derived suppressor cells (MDSCs), and it upregulates MHC class I and E-cadherin expression in tumor cells. It shows antitumor efficacy in syngeneic mouse tumor models and is used in research on breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma[1][2]. It is supplied as an off-white to light yellow solid (C27H25F6N5O7, MW 645.51) at 99.82% purity.
Physical & Chemical Properties
| Molecular Formula | C27H25F6N5O7 |
|---|---|
| Molecular Weight | 645.51 g/mol |
| Purity | 99.82% |
| Appearance | Solid |
| Color | Off-white to light yellow |
| SMILES | O=C(C1=NN(CCC)C=C1OCC(F)(F)F)NC2=NC=C(C=C2)OC3=C4C=C(OC)C(OC)=CC4=NC=C3.OC(C(F)(F)F)=O |
| Target | Axl, Mer, MHC I |
| Signaling Pathway | Protein Tyrosine Kinase/RTK; Immunology/Inflammation |
| Solubility | In Vitro: DMSO: 100 mg/mL (154.92 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | 4°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
Activity & Target
|
Axl 0.3 nM (Kd) |
Mer 0.8 nM (Kd) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
[2]. NAM K, et al. Quinoline derivatives as inhibitors of axl/mer rtk and csf1r. WO, WO2019229251A1, 2019-12-05.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (154.92 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
Data provided by the manufacturer.
In Vitro
Adrixetinib (Q702; 1 h) TFA binds purified Axl, Mer, and CSF1R kinases potently and inhibits them, with respective IC50 values of 0.3 nM, 0.8 nM, and 8.7 nM[1]. In H1299 cells, Adrixetinib (0.001-10 μM; 24 h pretreatment) TFA inhibits Gas6-induced phosphorylation of Axl and AKT in a concentration-dependent manner. In A549 cells, it likewise inhibits Gas6-induced phosphorylation of Mer and AKT in a concentration-dependent manner, and in THP-1 cells it inhibits CSF1-induced phosphorylation of CSF1R and ERK in a concentration-dependent manner[1]. Adrixetinib (0.1-100 μM; 72 h) TFA directly reduces EMT6 cell viability, with an IC50 of 8.4 μM[1]. Via the CSF1R pathway, Adrixetinib TFA suppresses M-NFS-60 cell proliferation with an IC50 < 1.0 μM, indicating potent cellular activity[2].
In Vivo
In nude mice bearing subcutaneous xenograft tumors, Adrixetinib TFA (Q702; 30 mg/kg; p.o.; daily; 7 days) blocks phosphorylation of Axl and CSF1R[1]. Adrixetinib (10-100 mg/kg; p.o.; daily; 14 days) TFA produces dose-dependent control of tumor growth (54.3% to 84.6%) in syngeneic subcutaneous EMT6 breast cancer tumors in BALB/c mice[1]. In BALB/c mice with subcutaneous EMT6 tumors, Adrixetinib TFA (30 mg/kg; p.o.; daily; up to 7 days) modulates EMT6 gene expression, promoting an immune-stimulatory microenvironment[1]. In BALB/c mice, Adrixetinib TFA (30 mg/kg; p.o.; daily; 5 to 22 days) brings about remodeling of the immune cell population in subcutaneous MHC-I as well as E-cadherin expression[1]. Effector function of T and natural killer cells is enhanced in BALB/c mice by Adrixetinib (30 mg/kg; p.o.; daily; 7 days) TFA, which raises IFN-γ and granzyme B production in subcutaneous EMT6 tumors as well as in peripheral blood[1]. CD8 T cell infiltration is raised, myeloid cell accumulation is lowered, and MHC-I and PD-L1 expression is upregulated by Adrixetinib (30 mg/kg; p.o.; daily; 21 days) TFA in subcutaneous EMT6 tumors of BALB/c mice[1]. Adrixetinib (30 mg/kg; p.o.; daily; 9 days) TFA raises the infiltration of tumor antigen-specific CD8 T cells into subcutaneous B16F10-OVA melanoma tumors in C57BL/6 mice[1]. In mice with subcutaneous CT26, MC38, and RENCA syngeneic tumor models, Adrixetinib (30 mg/kg; p.o.; daily; up to 27 days) TFA brings about tumor growth inhibition (64% to 77% TGI)[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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