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Pfizer Inc axitinib
Axitinib, supplied by Pfizer Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/axitinib/axitinib/us12551564-1110-10-12
Average 86 stars, based on 1 article reviews
axitinib - by Bioz Stars, 2026-09
86/100 stars

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Article Title: IRAK degraders and uses thereof
Article Snippet: VEGFR inhibitors, such as regorafenib (Stivarga®, Bayer); vandetanib (Caprelsa®, AstraZeneca); axitinib (Inlyta®, Pfizer); and lenvatinib (Lenvima®, Eisai); Raf inhibitors, such as sorafenib (Nexavar®, Bayer AG and Onyx); dabrafenib (Tafinlar®, Novartis); and vemurafenib (Zelboraf®, Genentech/Roche); MEK inhibitors, such as cobimetanib (Cotellic®, Exelexis/Genentech/Roche); trametinib (Mekinist®, Novartis); Bcr-Abl tyrosine kinase inhibitors, such as imatinib (Gleevec®, Novartis); nilotinib (Tasigna®, Novartis); dasatinib (Sprycel®, BristolMyersSquibb); bosutinib (Bosulif®, Pfizer); and ponatinib (Inclusig®, Ariad Pharmaceuticals); Her2 and EGFR inhibitors, such as gefitinib (Iressa®, AstraZeneca); erlotinib (Tarceeva®, Genentech/Roche/Astellas); lapatinib (Tykerb®, Novartis); afatinib (Gilotrif®, Boehringer Ingelheim); osimertinib (targeting activated EGFR, Tagrisso®, AstraZeneca); and brigatinib (Alunbrig®, Ariad Pharmaceuticals); c-Met and VEGFR2 inhibitors, such as cabozanitib (Cometriq®, Exelexis); and multikinase inhibitors, such as sunitinib (Sutent®, Pfizer); pazopanib (Votrient®, Novartis); ALK inhibitors, such as crizotinib (Xalkori®, Pfizer); ceritinib (Zykadia®, Novartis); and alectinib (Alecenza®, Genentech/Roche); Bruton's tyrosine kinase inhibitors, such as ibrutinib (Imbruvica®, Pharmacyclics/Janssen); and Flt3 receptor inhibitors, such as midostaurin (Rydapt®, Novartis).

Article Title: Protein degraders and uses thereof
Article Snippet: VEGFR inhibitors, such as regorafenib (Stivarga®, Bayer); vandetanib (Caprelsa®, AstraZeneca); axitinib (Inlyta®, Pfizer); and lenvatinib (Lenvima®, Eisai); Raf inhibitors, such as sorafenib (Nexavar®, Bayer AG and Onyx); dabrafenib (Tafinlar®, Novartis); and vemurafenib (Zelboraf®, Genentech/Roche); MEK inhibitors, such as cobimetanib (Cotellic®, Exelexis/Genentech/Roche); trametinib (Mekinist®, Novartis); Bcr-Abl tyrosine kinase inhibitors, such as imatinib (Gleevec®, Novartis); nilotinib (Tasigna®, Novartis); dasatinib (Sprycel®, BristolMyersSquibb); bosutinib (Bosulif®, Pfizer); and ponatinib (Inclusig®, Ariad Pharmaceuticals); Her2 and EGFR inhibitors, such as gefitinib (Iressa®, AstraZeneca); erlotinib (Tarceeva®, Genentech/Roche/Astellas); lapatinib (Tykerb®, Novartis); afatinib (Gilotrif®, Boehringer Ingelheim); osimertinib (targeting activated EGFR, Tagrisso®, AstraZeneca); and brigatinib (Alunbrig®, Ariad Pharmaceuticals); c-Met and VEGFR2 inhibitors, such as cabozanitib (Cometriq®, Exelexis); and multikinase inhibitors, such as sunitinib (Sutent®, Pfizer); pazopanib (Votrient®, Novartis); ALK inhibitors, such as crizotinib (Xalkori®, Pfizer); ceritinib (Zykadia®, Novartis); and alectinib (Alecenza®, Genentech/Roche); Bruton's tyrosine kinase inhibitors, such as ibrutinib (Imbruvica®, Pharmacyclics/Janssen); and Flt3 receptor inhibitors, such as midostaurin (Rydapt®, Novartis).

Article Title: CDK2 inhibitors
Article Snippet: Preferred anti-angiogenesis agents include sunitinib (SutentTM), bevacizumab (AvastinTM), axitinib (AG 13736), SU 14813 (Pfizer), and AG 13958 (Pfizer).

Article Title: IRAK degraders and uses thereof
Article Snippet: VEGFR inhibitors, such as regorafenib (Stivarga®, Bayer); vandetanib (Caprelsa®, AstraZeneca); axitinib (Inlyta®, Pfizer); and lenvatinib (Lenvima®, Eisai); Raf inhibitors, such as sorafenib (Nexavar®, Bayer AG and Onyx); dabrafenib (Tafinlar®, Novartis); and vemurafenib (Zelboraf®, Genentech/Roche); MEK inhibitors, such as cobimetanib (Cotellic®, Exelexis/Genentech/Roche); trametinib (Mekinist®, Novartis); Bcr-Abl tyrosine kinase inhibitors, such as imatinib (Gleevec®, Novartis); nilotinib (Tasigna®, Novartis); dasatinib (Sprycel®, BristolMyersSquibb); bosutinib (Bosulif®, Pfizer); and ponatinib (Inclusig®, Ariad Pharmaceuticals); Her2 and EGFR inhibitors, such as gefitinib (Iressa®, AstraZeneca); erlotinib (Tarceeva®, Genentech/Roche/Astellas); lapatinib (Tykerb®, Novartis); afatinib (Gilotrif®, Boehringer Ingelheim); osimertinib (targeting activated EGFR, Tagrisso®, AstraZeneca); and brigatinib (Alunbrig®, Ariad Pharmaceuticals); c-Met and VEGFR2 inhibitors, such as cabozanitib (Cometriq®, Exelexis); and multikinase inhibitors, such as sunitinib (Sutent®, Pfizer); pazopanib (Votrient®, Novartis); ALK inhibitors, such as crizotinib (Xalkori®, Pfizer); ceritinib (Zykadia®, Novartis); and alectinib (Alecenza®, Genentech/Roche); Bruton's tyrosine kinase inhibitors, such as ibrutinib (Imbruvica®, Pharmacyclics/Janssen); and Flt3 receptor inhibitors, such as midostaurin (Rydapt®, Novartis).

Article Title: SMARCA degraders and uses thereof
Article Snippet: VEGFR inhibitors, such as regorafenib (Stivarga®, Bayer); vandetanib (Caprelsa®, AstraZeneca); axitinib (Inlyta®, Pfizer); and lenvatinib (Lenvima®, Eisai); Raf inhibitors, such as sorafenib (Nexavar®, Bayer AG and Onyx); dabrafenib (Tafinlar®, Novartis); and vemurafenib (Zelboraf®, Genentech/Roche); MEK inhibitors, such as cobimetanib (Cotellic®, Exelexis/Genentech/Roche); trametinib (Mekinist®, Novartis); Bcr-Abl tyrosine kinase inhibitors, such as imatinib (Gleevec®, Novartis); nilotinib (Tasigna®, Novartis); dasatinib (Sprycel®, BristolMyersSquibb); bosutinib (Bosulif®, Pfizer); and ponatinib (Inclusig®, Ariad Pharmaceuticals); Her2 and EGFR inhibitors, such as gefitinib (Iressa®, AstraZeneca); erlotinib (Tarceeva®, Genentech/Roche/Astellas); lapatinib (Tykerb®, Novartis); afatinib (Gilotrif®, Boehringer Ingelheim); osimertinib (targeting activated EGFR, Tagrisso®, AstraZeneca); and brigatinib (Alunbrig®, Ariad Pharmaceuticals); c-Met and VEGFR2 inhibitors, such as cabozanitib (Cometriq®, Exelexis); and multikinase inhibitors, such as sunitinib (Sutent®, Pfizer); pazopanib (Votrient®, Novartis); ALK inhibitors, such as crizotinib (Xalkori®, Pfizer); ceritinib (Zykadia®, Novartis); and alectinib (Alecenza®, Genentech/Roche); Bruton's tyrosine kinase inhibitors, such as ibrutinib (Imbruvica®, Pharmacyclics/Janssen); and Flt3 receptor inhibitors, such as midostaurin (Rydapt®, Novartis).

Article Title: Functionally characterizing the renal cell carcinoma tumor immune microenvironment via patient-derived ex vivo models
Article Snippet: 772 We acknowledge Pfizer Oy, Helsinki Finland for Axitinib as an in-kind contribution 773 as part of the grant #54497481.

Article Title: Methods of treating cytokine release syndrome by administering a molecule comprising a soluble tandem selectin glycoprotein ligand
Article Snippet: Protein kinase inhibitors or VEGF-R antagonists useful in the present invention include axitinib (Inlvta®, Pfizer Inc., NY, USA), sorafenib (Nexavar®, Bayer AG and Onyx); sunitinib (Sutent®, Pfizer, New York, US); pazopanib (Votrient®, GlaxoSmithKline, Research Triangle Park, US); cabozanitib (Cometriq®, Exelexis, US); regorafenib (Stivarga®, Bayer); lenvatinib (Lenvima®, Eisai); bevacizumab (Avastin®, Genentech, Inc. of South San Francisco, Calif.), an anti-VEGF monoclonal antibody: and aflibercept, also known as VEGF Trap (Zaltrap®; Regeneron/Sanofi).

Article Title: Use of caseinolytic protease P function as a biomarker of drug response to imipridone-like agents
Article Snippet: Preferred anti-angiogenesis agents include sunitinib (Sutent®), bevacizumab (Avastin®), axitinib (AG 13736), SU 14813 (Pfizer), and AG 13958 (Pfizer).



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Assessment of the tube formation capability, CD31 and <t>VEGF</t> gene expressions for HUVECs treated without (control) and with cell culture supernatant collected <t>from</t> <t>H-EMSCs</t> seeded on PCL-HA (PCL-HA/H-E) or H-EMSCs and mø co-seeded on PCL-HA (PCL-HA/H-E/mø). A Tube formation assay of HUVECs in the control, PCL-HA/H-E and PCL-HA/H-E/mø groups. Scale bar = 200 μm. B Quantification of the total length of the tubes formed. C Quantification of the total number of meshes formed. D Quantification of the number of nodes formed. E CD31 gene expression of the HUVECs. F VEGF gene expression of the HUVECs. *** p < 0.001. ## p < 0.01, ### p < 0.001 vs. Control
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Assessment of the tube formation capability, CD31 and VEGF gene expressions for HUVECs treated without (control) and with cell culture supernatant collected from H-EMSCs seeded on PCL-HA (PCL-HA/H-E) or H-EMSCs and mø co-seeded on PCL-HA (PCL-HA/H-E/mø). A Tube formation assay of HUVECs in the control, PCL-HA/H-E and PCL-HA/H-E/mø groups. Scale bar = 200 μm. B Quantification of the total length of the tubes formed. C Quantification of the total number of meshes formed. D Quantification of the number of nodes formed. E CD31 gene expression of the HUVECs. F VEGF gene expression of the HUVECs. *** p < 0.001. ## p < 0.01, ### p < 0.001 vs. Control

Journal: Stem Cell Research & Therapy

Article Title: Co-delivery of endometrial mesenchymal stem cells and macrophages by an electrospun patch promotes angiogenesis during endometrial injury repair via VEGF related signalling

doi: 10.1186/s13287-026-04929-2

Figure Lengend Snippet: Assessment of the tube formation capability, CD31 and VEGF gene expressions for HUVECs treated without (control) and with cell culture supernatant collected from H-EMSCs seeded on PCL-HA (PCL-HA/H-E) or H-EMSCs and mø co-seeded on PCL-HA (PCL-HA/H-E/mø). A Tube formation assay of HUVECs in the control, PCL-HA/H-E and PCL-HA/H-E/mø groups. Scale bar = 200 μm. B Quantification of the total length of the tubes formed. C Quantification of the total number of meshes formed. D Quantification of the number of nodes formed. E CD31 gene expression of the HUVECs. F VEGF gene expression of the HUVECs. *** p < 0.001. ## p < 0.01, ### p < 0.001 vs. Control

Article Snippet: For the VEGF inhibition experiments, 18 female SD rats in estrus were divided into the following three groups, with 6 rats in each group: PCL-HA/H-E group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs) was transplanted; PCL-HA/H-E/mø group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs + 0.25 × 10 6 mø) was transplanted; PCL-HA/H-E/mø/VEGF inhibitor group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs and 0.25 × 10 6 mø) was implanted, VEGF inhibitor (Axitinib (HY-10065, MCE), 100 mg/kg) was injected into the rat uterine cavity.

Techniques: Control, Cell Culture, Tube Formation Assay, Gene Expression

Assessment of the tube formation capability, CD31 and VEGF gene expressions of HUVECs treated with cell culture supernatant collected from H-EMSCs seeded on PCL-HA (PCL-HA/H-E) or H-EMSCs and mø co-seeded on PCL-HA (PCL-HA/H-E/mø) or H-EMSCs and mø co-seeded on PCL-HA and VEGF inhibitor (PCL-HA/H-E/mø/VEGF inhibitor). A Tube formation assay of HUVECs in the PCL-HA/H-E, PCL-HA/H-E/mø and PCL-HA/H-E/mø/VEGF inhibitor groups. Scale bar = 200 μm. B Quantification of the total length of the tubes formed. C Quantification of the total number of meshes formed. D Quantification of the number of nodes formed. E CD31 gene expression of the HUVECs. F VEGF gene expression of the HUVECs. *** p < 0.001. # p < 0.05, ### p < 0.001 vs. PCL-HA/H-E group

Journal: Stem Cell Research & Therapy

Article Title: Co-delivery of endometrial mesenchymal stem cells and macrophages by an electrospun patch promotes angiogenesis during endometrial injury repair via VEGF related signalling

doi: 10.1186/s13287-026-04929-2

Figure Lengend Snippet: Assessment of the tube formation capability, CD31 and VEGF gene expressions of HUVECs treated with cell culture supernatant collected from H-EMSCs seeded on PCL-HA (PCL-HA/H-E) or H-EMSCs and mø co-seeded on PCL-HA (PCL-HA/H-E/mø) or H-EMSCs and mø co-seeded on PCL-HA and VEGF inhibitor (PCL-HA/H-E/mø/VEGF inhibitor). A Tube formation assay of HUVECs in the PCL-HA/H-E, PCL-HA/H-E/mø and PCL-HA/H-E/mø/VEGF inhibitor groups. Scale bar = 200 μm. B Quantification of the total length of the tubes formed. C Quantification of the total number of meshes formed. D Quantification of the number of nodes formed. E CD31 gene expression of the HUVECs. F VEGF gene expression of the HUVECs. *** p < 0.001. # p < 0.05, ### p < 0.001 vs. PCL-HA/H-E group

Article Snippet: For the VEGF inhibition experiments, 18 female SD rats in estrus were divided into the following three groups, with 6 rats in each group: PCL-HA/H-E group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs) was transplanted; PCL-HA/H-E/mø group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs + 0.25 × 10 6 mø) was transplanted; PCL-HA/H-E/mø/VEGF inhibitor group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs and 0.25 × 10 6 mø) was implanted, VEGF inhibitor (Axitinib (HY-10065, MCE), 100 mg/kg) was injected into the rat uterine cavity.

Techniques: Cell Culture, Tube Formation Assay, Gene Expression

VEGF, CD31 gene and protein expression of rat endometrial tissues of the PCL-HA/H-E, PCL-HA/H-E/mø and PCL-HA/H-E/mø/VEGF inhibitor groups at day 7. A VEGF gene expression. B Quantification of VEGF protein concentration (pg/ml). C Representative images of VEGF immunostaining. Cell nuclei stained in blue while VEGF stained in red. Scale bar = 100 μm. D Quantification of VEGF staining area (%). E CD31 gene expression. F Representative images of CD31 immunostaining. Cell nuclei stained in blue while CD31 stained in red. Scale bar = 100 μm. G Quantification of CD31 staining area (%). *** p < 0.001. ## p < 0.01, ### p < 0.001 vs. PCL-HA/H-E group

Journal: Stem Cell Research & Therapy

Article Title: Co-delivery of endometrial mesenchymal stem cells and macrophages by an electrospun patch promotes angiogenesis during endometrial injury repair via VEGF related signalling

doi: 10.1186/s13287-026-04929-2

Figure Lengend Snippet: VEGF, CD31 gene and protein expression of rat endometrial tissues of the PCL-HA/H-E, PCL-HA/H-E/mø and PCL-HA/H-E/mø/VEGF inhibitor groups at day 7. A VEGF gene expression. B Quantification of VEGF protein concentration (pg/ml). C Representative images of VEGF immunostaining. Cell nuclei stained in blue while VEGF stained in red. Scale bar = 100 μm. D Quantification of VEGF staining area (%). E CD31 gene expression. F Representative images of CD31 immunostaining. Cell nuclei stained in blue while CD31 stained in red. Scale bar = 100 μm. G Quantification of CD31 staining area (%). *** p < 0.001. ## p < 0.01, ### p < 0.001 vs. PCL-HA/H-E group

Article Snippet: For the VEGF inhibition experiments, 18 female SD rats in estrus were divided into the following three groups, with 6 rats in each group: PCL-HA/H-E group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs) was transplanted; PCL-HA/H-E/mø group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs + 0.25 × 10 6 mø) was transplanted; PCL-HA/H-E/mø/VEGF inhibitor group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs and 0.25 × 10 6 mø) was implanted, VEGF inhibitor (Axitinib (HY-10065, MCE), 100 mg/kg) was injected into the rat uterine cavity.

Techniques: Expressing, Gene Expression, Protein Concentration, Immunostaining, Staining

H&E staining of rat endometrial tissues of the following groups: PCL-HA carrier with H-EMSCs mono-delivery (PCL-HA/H-E), PCL-HA carrier with H-EMSCs and mø co-delivery (PCL-HA/H-E/mø) and PCL-HA/H-E/mø with VEGF inhibitor (PCL-HA/H-E/mø/VEGF inhibitor), at day 7. A Representative H&E images of the rat endometrial tissues of the different treatment groups at day 7. Scale bar = 560 μm. Enlarged images are shown at the bottom and scale bar = 220 μm. B Quantification of the endometrium thickness. C Quantification of the number of endometrial glands. *** p < 0.001, ## p < 0.01, ### p < 0.001 vs. PCL-HA/H-E group

Journal: Stem Cell Research & Therapy

Article Title: Co-delivery of endometrial mesenchymal stem cells and macrophages by an electrospun patch promotes angiogenesis during endometrial injury repair via VEGF related signalling

doi: 10.1186/s13287-026-04929-2

Figure Lengend Snippet: H&E staining of rat endometrial tissues of the following groups: PCL-HA carrier with H-EMSCs mono-delivery (PCL-HA/H-E), PCL-HA carrier with H-EMSCs and mø co-delivery (PCL-HA/H-E/mø) and PCL-HA/H-E/mø with VEGF inhibitor (PCL-HA/H-E/mø/VEGF inhibitor), at day 7. A Representative H&E images of the rat endometrial tissues of the different treatment groups at day 7. Scale bar = 560 μm. Enlarged images are shown at the bottom and scale bar = 220 μm. B Quantification of the endometrium thickness. C Quantification of the number of endometrial glands. *** p < 0.001, ## p < 0.01, ### p < 0.001 vs. PCL-HA/H-E group

Article Snippet: For the VEGF inhibition experiments, 18 female SD rats in estrus were divided into the following three groups, with 6 rats in each group: PCL-HA/H-E group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs) was transplanted; PCL-HA/H-E/mø group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs + 0.25 × 10 6 mø) was transplanted; PCL-HA/H-E/mø/VEGF inhibitor group: PCL-HA electrospun carrier (1 × 10 6 H-EMSCs and 0.25 × 10 6 mø) was implanted, VEGF inhibitor (Axitinib (HY-10065, MCE), 100 mg/kg) was injected into the rat uterine cavity.

Techniques: Staining