Thyroid cancers are tumours of the thyroid gland, and originate from follicular or parafollicular cells. These are often caused by radiation exposure, and can present as a nodule in the anterior region of the neck.
Causes
Thyroid cancer can occur in people of any age.
Radiation increases the risk of developing thyroid cancer. Exposure may occur from:
1.Radiation therapy to the neck (especially in childhood)
2.Radiation exposure from nuclear plant disasters
Other risk factors are a family history of thyroid cancer and chronic goiter (enlarged thyroid).
There are several types of thyroid cancer:
1.Anaplastic carcinoma (also called giant and spindle cell cancer) is the most dangerous form of thyroid cancer. It is rare, and spreads quickly.
2.Follicular tumor is more likely to come back and spread.
3.Medullary carcinoma is a cancer of non-thyroid cells that are normally present in the thyroid gland. This form of thyroid cancer tends to occur in families.
4.Papillary carcinoma is the most common type, and it usually affects women of childbearing age. It spreads slowly and is the least dangerous type of thyroid cancer.
Cat. No. | Product Name | CAS No. | Information |
---|---|---|---|
H8129 |
Vandetanib trifluoroacetate |
338992-53-3 | A potent and selective VEGFR2 (KDR) inhibitor with IC50 of 40 nM; shows weak inhibition for VEGFR3 and EGFR (IC50 is 100 nM and 500 nM respectively); displays excellent selectivity over erbB2, MEK, CDK-2, Tie-2, IGFR-1R, PDK, PDGFRβ, and Akt (IC50=1.1-100 uM); has excellent solubility and good oral bioavailability. |
H8128 |
Vandetanib hydrochloride |
524722-52-9 | A potent and selective VEGFR2 (KDR) inhibitor with IC50 of 40 nM; shows weak inhibition for VEGFR3 and EGFR (IC50 is 100 nM and 500 nM respectively); displays excellent selectivity over erbB2, MEK, CDK-2, Tie-2, IGFR-1R, PDK, PDGFRβ, and Akt (IC50=1.1-100 uM); has excellent solubility and good oral bioavailability. |
H8127 |
Vandetanib |
443913-73-3 | A potent and selective VEGFR2 (KDR) inhibitor with IC50 of 40 nM; shows weak inhibition for VEGFR3 and EGFR (IC50 is 100 nM and 500 nM respectively); displays excellent selectivity over erbB2, MEK, CDK-2, Tie-2, IGFR-1R, PDK, PDGFRβ, and Akt (IC50=1.1-100 uM); has excellent solubility and good oral bioavailability. |
H7961 |
Pralsetinib |
2097132-94-8 |
BLU-667 (Pralsetinib, BLU667) is a highly potent, selective, next generation RET inhibitor with IC50 of 0.3-0.4 nM for WT RET, RET mutants V804L, V804M, M918T and CCDC6-RET fusion; displays 8- to 28-fold more potent against WT RET than cabozantinib, vandetanib, and RXDX-105; shows 88-fold selectivity over VEGFR-2, >100-fold more selective for RET over 96% of kinases in a panel of 371 kinases; inhibits RET autophosphorylation with cellular IC50 of 5 nM, at least 10 times more potently than cabozantinib, vandetanib, and RXDX-105; inhibits phosphorylation of RET, SHC, and ERK1/2 in a panel of RET-driven cell lines at <10 nM, suppresses proliferation of KIF5B-RET Ba/F3 cells harboring V804L, V804M, or V804E variants as potently as WT RET; demonstrates antitumor activity on diverse RET-driven in vivo models. |
H7853 |
Varlitinib |
845272-21-1 |
Varlitinib (ARRY-334543) is a?potent, orally active, ATP-competitive, selective, reversible inhibitor of ErbB1 and ErbB2; significantly reverses ABCG2-MDR by directly inhibiting the drug efflux function of ABCG2 at 1.0 uM; significantly reverses drug resistance mediated by ABCG2. |
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