KP1019  (Synonyms: FFC14A)

KP1019 (FFC14A) is a Ru(III)-based anti-metastatic and cytotoxic anti-cancer agent. KP1019 induces DNA damage and apoptosis in cancer cells^[1][2].

KP1019 is internalized by yeast and induces mutations, cell cycle delay, and cell death. KP1019 sensitivity of strains defective in DNA repair is examined, ultimately showing that rad1Δ, rev3Δ, and rad52Δ yeast are hypersensitive to KP1019, suggesting that nucleotide excision repair (NER), translesion synthesis (TLS), and recombination each play a role in drug tolerance^[1].
KP1019 inhibits proliferation of ovarian tumor cells, induces DNA damage and apoptosis in colon carcinoma cells. KP1019 causes interstrand cross-links and bulky DNA adducts in mammalian cell lines^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

KP1019 treatment inhibits primary tumour growth in in the model of MCa mammary carcinoma. None of the treatments reduced the development of lung metastatases in this tumour model^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

598.30

C₂₁H₁₉Cl₄N₆Ru

124875-20-3

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Shannon K Stevens, et al. The anticancer ruthenium complex KP1019 induces DNA damage, leading to cell cycle delay and cell death in Saccharomyces cerevisiae. Mol Pharmacol. 2013 Jan;83(1):225-34.  [Content Brief]

  [2]. Gemma K Gransbury, et al. Comparison of KP1019 and NAMI-A in tumour-mimetic environments. Metallomics. 2016 Aug 1;8(8):762-73.  [Content Brief]

  [3]. A Bergamo, et al. Inhibitory Effects of the Ruthenium Complex KP1019 in Models of Mammary Cancer Cell Migration and Invasion. Met Based Drugs. 2009;2009:681270.  [Content Brief]