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Medication: Nanoparticles for Imaging and Drug Delivery
Published in Harry F. Tibbals, Medical Nanotechnology and Nanomedicine, 2017
NK012 is another polymeric micelle drug formulation loaded with the iri-notecan metabolite SN-38, with two Phase II clinical trials for breast and lung cancer (2009). SN-38 (7-ethyl-10-hydroxy-camptothecin) is a biologically active metabolite of the prodrug irinotecan (CPT-11), which binds to and inhibits topoisomerase I by stabilizing the cleavable complex between topoi-somerase I and DNA, resulting in DNA breaks, inhibition of DNA replication, and apoptosis. SN-38 has been reported to exhibit up to 1000-fold more cytotoxic activity against various cancer cells in vitro than irinotecan. This SN-38-releasing nanodevice is constructed by covalently attaching SN-38 to the block copolymer PEG-PGlu, followed by self-assembly of amphiphilic block copolymers in an aqueous milieu. This formulation increases the water solubility of SN-38 and allows the delivery of higher doses of SN-38 than those achievable with SN-38 alone [183].
Buthionine sulfoximine and chemoresistance in cancer treatments: a systematic review with meta-analysis of preclinical studies
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Camila dos Reis Oliveira, Joedna Cavalcante Pereira, Andressa Barros Ibiapina, Italo Rossi Roseno Martins, João Marcelo de Castro e Sousa, Paulo Michel Pinheiro Ferreira, Felipe Cavalcanti Carneiro da Silva
For in vitro cytotoxicity assays, the chemotherapeutics and other pharmacological agents most frequently used in association with BSO were: Natural products (n = 19) and antibiotics (n = 12): arsenic trioxide (ATO), L-asparaginase, sesquiterpene lactones, SN-38 (active metabolite of irinotecan), hydroxychavicol, etoposide, vincristine, ferrous gallic acid, paclitaxel, eupatoriopicrin, menadione, helenalin, doxorubicin, daunorubicin, mitomycin C, actinomycin;Alkylating agents (n = 15) and platinum analogues (n = 12): melphalan (L-PAM), carmustine (BCNU), temozolomide, cisplatin (CDDP), cyclophosphamide (CFA), nitrogen mustard, iproplatin, oxaliplatin;Antimetabolics (n = 4): 5-fluorouracil, gemcitabine, azathioprine;Other pharmacological agents (n = 39): auranofin, erlotinib, perifosine, protoporphyrin Zn(II), arsenic disulfide, sahaquin, photosensitizers (chlorine e6, phthalocyanine aluminum disulfonate), sulindac sulfide, ATN-224, misonidazole, 2-deoxyglucose (2DG), organometallic complexes, 17 -(allylamino)-17-demethoxygeldanamycin (17AAG), TNF-α, fenretinide, gold nanoparticles, erastine, calcitriol, sodium butyrate, 3-bromopyruvate, inhibitors of antioxidant molecules (2-methoxyestradiol, 3-amino-1,2,4-triazole, diethylmaleate), L-dopa, naphthols, prednisolone, metallointercalators, MRP1 modulator, nifurtimox, hydroquinone, N-acetyl-4-S-cysteaminylphenol (NA-CAP).
Pharmacokinetics of α-amanitin in mice using liquid chromatography-high resolution mass spectrometry and in vitro drug–drug interaction potentials
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Ria Park, Won-Gu Choi, Min Seo Lee, Yong-Yeon Cho, Joo Young Lee, Han Chang Kang, Chang Hwan Sohn, Im-Sook Song, Hye Suk Lee
α-Amanitin did not markedly inhibit UGT1A1-catalyzed SN-38 glucuronidation, UGT1A3-catalyzed chenodeoxycholic acid 24-acyl-β-glucuronidation, UGT1A4-catalyzed trifluoperazine N-β-D-glucuronidation, UGT1A6-catalyzed N-acetylserotonin β-D-glucuronidation, UGT1A9-catalyzed mycophenolic acid β-D-glucuronidation, and UGT2B7-catalyzed naloxone 3-β-D-glucuronidation at 50 μM in HLMs (Figure 5).