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Targeted Therapy for Kidney Cancer

Targeted Therapy
What is Targeted Therapy
Targeted Therapy: Targets
Targeted Therapy for Cancer
- Targeted Therapy for Kidney Cancer
- Targeted Therapy for Liver Cancer
- Colorectal Cancer Targeted Therapy
- What is Targeted Therapy for Cancer
- Targeted Therapy for Leukemia
-- Targeted Therapy for Acute Lymphocytic Leukemia
-- Targeted Therapy for Chronic Lymphocytic Leukemia
-- Targeted Therapy for Chronic Myeloid Leukemia
-- Targeted Therapy for Acute Myeloid Leukemia
- Targeted Therapy for Pancreatic Cancer
- Prostate Cancer Targeted Therapy
- Targeted Therapy for Ovarian Cancer
- Melanoma Targeted Therapy
- Targeted Therapy for Lung Cancer
-- Non-Small Cell Lung Cancer (NSCLC) Targeted Therapy
-- Small Cell Lung Cancer Targeted Therapy
-- EGFR Targeted Therapy Lung Cancer
- Targeted Therapy for Breast Cancer
-- Targeted Therapy for Hormone Receptor Positive Breast Cancer
-- Targeted Therapy for HER2 Positive Breast Cancer
-- Targeted Therapy for Triple-Negative Breast Cancer
-- What is Targeted Therapy for Breast Cancer
EGFR Targeted Therapy
HER2 Targeted Therapy
VEGF Targeted Therapy
BRAF Targeted Therapy
ALK Targeted Therapy
Immune Checkpoint Targeted Therapy
Targeted Therapy Drugs
The Differences between Chemotherapy and Targeted Therapy
Side Effects of Targeted Therapy
Oral Targeted Therapy
Targeted Therapy Resistance
How does Targeted Therapy Work
Immunotherapy
Cancer Immunotherapy
Immune checkpoint

Targeted Therapy for Kidney Cancer: Introduction

A wide variety of targeted therapies are available for the treatment of kidney cancer. The identified targeted therapies work by disrupting specific signalling pathways involved in tumour progression, such as those responsible for angiogenesis and cell proliferation. Tyrosine kinase inhibitors and mammalian target of rapamycin inhibitors are now established classes of drugs used in the treatment of kidney cancer, with a many of them having received regulatory approval to date. such as sorafenib, sunitinib, pazopanib, axitinib, temsirolimus, and everolimus).

Targeted Therapy for Kidney Cancer: Tyrosine Kinase Inhibitors (TKIs)

Tyrosine kinase inhibitors (TKIs) are small molecules that inhibit a variety of different signalling molecule receptors, including VEGFR-1, VEGFR-2, and VEGFR-3; PDGFR-α and PDGFR-β; c-RET; macrophage colony-stimulating factor (CSF-1R); FMS-like tyrosine kinase-3 receptor (Flt-3); and c-KIT. This activity provides them with the potential to disrupt a range of tumour angiogenesis signalling pathways.
Sorafenib is an orally active TKI that been shown to exhibit inhibitory effects against VEGFR-2 and VEGFR-3, PDGFR-β, Flt-3, RAF-1, and c-KIT.
Sunitinib is also an orally active TKI and has affinity for VEGFR-2, Flt-3, c-KIT, and PDGFR-β.
Pazopanib is orally active and has been shown to inhibit VEGFR-1, VEGFR-2, and VEGFR-3; PDGFR-α and PDGFR-β; and c-KIT.
Axitinib has been shown to be highly selective for inhibition of VEGFR-1, VEGFR-2, and VEGFR-3 over other compounds such as PDGFRs and KIT.
Tivozanib is an orally active TKI and, as with axitinib, has inhibitory activity against VEGFR-1, VEGFR-2, and VEGFR-3.
Dovitinib is an orally active TKI that has activity against VEGFR, FGFR, and PDGFR.
Regorafenib is an orally available TKI that is known to inhibit VEGFR-1, VEGFR-2, and VEGFR-3, as well as PDGFR-β, FGFR-1, Tie2, BRAF, RAF-1, and RET.
Cediranib has been shown to be highly potent in in vitro assays and pre-clinical models, inhibiting all three VEGF receptors.

Targeted Therapy for Kidney Cancer: Mammalian Target of Rapamycin (mTOR) Inhibitors

Rapamycin was initially investigated as an immunosuppressant owing to its ability to inhibit T cell function for organ transplant patients. It was subsequently identified as having anti-proliferative effects in a number of malignancies. Rapamycin binds to the intracellular FK506 binding protein 12 (FKBP12), and the resulting protein–drug complex inhibits mTOR kinase activity. To date, there are two mTOR inhibitors that are approved for use in the treatment of advanced kidney cancer, temsirolimus, and everolimus.
Temsirolimus is a pro-drug of rapamycin that is rapidly metabolised in the liver by cytochrome CYP 4503A4/5 to the active form. It has better chemical stability and solubility than rapamycin does, making it suitable for intravenous administration.
Everolimus is an orally available hydroxyethyl ether derivative that does not require in vivo transformation to sirolimus in order to be active.

Targeted Therapy for Kidney Cancer: Reference

Minguet J, Smith K H, Bramlage C P, et al. Targeted therapies for treatment of renal cell carcinoma: recent advances and future perspectives[J]. Cancer chemotherapy and pharmacology, 2015, 76(2): 219-233.

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