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PNU-159682 Sale

目录号 : GC36941

PNU-159682是一种高效的蒽环类新霉素代谢产物,具有突出的细胞毒性,是一种有效的 ADC细胞毒素。

PNU-159682 Chemical Structure

Cas No.:202350-68-3

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥4,655.00
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1mg
¥2,074.00
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5mg
¥5,250.00
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10mg
¥7,000.00
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50mg
¥14,220.00
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Sample solution is provided at 25 µL, 10mM.

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实验参考方法

Kinase experiment:

The inhibition of topoisomerase II activity is tested by taking advantage of the ability of this enzyme to decatenate kinetoplast DNA (kDNA); the test is specific for both isoforms of topoisomerase II (α and β) because it relies on the conversion of catenated DNA to its decatenated form, which requires double strand cut and ligation uniquely performed by topoisomerase II. The DNA used in this test is the mitochondrial kDNA of Crithidia fasciculata, a catenated network of DNA rings, most of which are 2.5 kb monomers. The kDNA networks are large relative to the monomers and do not migrate in the gel remaining in the well, while the minicircles can be easily resolved in agarose gel. Both the gel and the running buffer contain the intercalator ethidium bromide, which allows the monitoring of monomers appearance with a UV light source and the resolution of different DNA forms (linear, nicked circular DNA, and relaxed DNA monomers), helping to clearly distinguish the linear DNA from the nicked circular DNA. In this test, 200 ng of kDNAs is incubated for 1 h at 37°C with doxorubicin at 10, 1, or 0.1 μM, or with PNU-159682 at 100, 10, or 1 μM in the presence of 0.025 U of human topoisomerase IIα in a topoisomerase II reaction buffer (Tris-HCl pH 7.9 40 mM, KCl 80 mM, DTT 5 mM, BSA 15 μg/mL, ATP 1 mM, and MgCl2 10 mM). At the end of the incubation period, each sample is spiked with 3 μL of gel loading buffer (xylene cyanol 0.25%, blue bromophenol 0.25%, Ficoll 400 18%, and EDTA 6 mM) and then analyzed by agarose (1%) gel electrophoresis. Runs are performed in TBE buffer (Tris 89 mM, boric Acid 89 mM, EDTA 2 mM, pH 8.0) in the presence of ethidium bromide 0.5 μg/mL. Samples are run overnight at 1 V/cm.

Cell experiment:

SKRC-52 cells are seeded in 96-well plates in RPMI added with 10% FCS (100 μL) at a density of 5000 cells per well and allowed to grow for 24 h. The medium is replaced with medium containing different concentrations of test substance (1:3 dilution steps) and plates are incubated under standard culture conditions. After 72 h the medium is removed, MTS cell viability dye (20 μL) in 150 μL of the medium is added, the plates are incubated for 2 h under culture conditions and the absorbance at 490 nm measured on a Spectra Max Paradigm multimode plate reader. Experiments are performed in triplicate and average cell viability calculated as measured background corrected absorbance divided by the absorbance of untreated control wells. IC50 values are determined by fitting data to the four-parameter logistic equation, using a Prism 6 software for data analysis.

Animal experiment:

Four- to six-week-old female CD-1 athymic nude mice are used for evaluation of the activity of PNU-159682 against MX-1 human mammary carcinoma xenografts. On day 0, animals (n=14) are grafted s.c. with MX-1 tumor fragments in the right flank. Eight days later, they are randomly assigned to the drug treatment group or control group (n=7 mice per group), and treatment is started. PNU-159682 is given i.v. (4 μg/kg) according to a q7dx3 (every 7 days for three doses) schedule; control animals receive saline injections. Tumor volume is estimated from measurements done with a caliper; where D and d are the longest and the shortest diameters, respectively. For ethical reasons, control animals are sacrificed on day 21 when the mean tumor volume in the group is appr 2,500 mm3; animals receiving drug treatment are monitored up to day 50, at which point they are sacrificed.

References:

[1]. Quintieri L, et al. Formation and antitumor activity of PNU-159682, a major metabolite of nemorubicin in human liver microsomes. Clin Cancer Res. 2005 Feb 15;11(4):1608-17.
[2]. Cazzamalli S, et al. Acetazolamide Serves as Selective Delivery Vehicle for Dipeptide-Linked Drugs to Renal Cell Carcinoma. Mol Cancer Ther. 2016 Dec;15(12):2926-2935.
[3]. Scalabrin M, et al. Virtual Cross-Linking of the Active Nemorubicin Metabolite PNU-159682 to Double-Stranded DNA. Chem Res Toxicol. 2017 Feb 20;30(2):614-624.

产品描述

PNU-159682, a highly potent metabolite of the anthracycline nemorubicin with outstanding cytotoxicity, is a potent ADCs cytotoxin.

PNU-159682 inhibits a panel of human tumor cell lines with IC70 values in the range of 0.07-0.58 nM, and is 2,360- to 790-fold and 6,420- to 2,100-fold more potent than MMDX and doxorubicin, respectively[1]. PNU-159682 (100 μM) weakly inhibits topoisomerase II unknotting activity. PNU-159682 (10 μM)-DNA adducts contain one or two drug molecules bound to double-stranded DNA[2]. PNU-159682 shows cytotoxic effect on CAIX-expressing SKRC-52 cells with IC50 of 25 nM[3].

PNU-159682 (15 μg/kg, i.v.) shows antitumor activity in mice bearing disseminated murine L1210 leukemia and in MX-1 human mammary carcinoma xenografts at 4 μg/kg[1]. PNU-159682 (25 nmol/kg) exhibits a potent antitumor effect in mice bearing SKRC-52 xenografted tumors[3].

[1]. Quintieri L, et al. Formation and antitumor activity of PNU-159682, a major metabolite of nemorubicin in human liver microsomes. Clin Cancer Res. 2005 Feb 15;11(4):1608-17. [2]. Scalabrin M, et al. Virtual Cross-Linking of the Active Nemorubicin Metabolite PNU-159682 to Double-Stranded DNA. Chem Res Toxicol. 2017 Feb 20;30(2):614-624. [3]. Cazzamalli S, et al. Acetazolamide Serves as Selective Delivery Vehicle for Dipeptide-Linked Drugs to Renal Cell Carcinoma. Mol Cancer Ther. 2016 Dec;15(12):2926-2935.

Chemical Properties

Cas No. 202350-68-3 SDF
Canonical SMILES COC1=C(C(C(C(O)=C([C@@H](O[C@H]2C[C@H]3[C@H](O[C@H]4N3CCO[C@@H]4OC)[C@H](C)O2)C[C@@](C(CO)=O)(O)C5)C5=C6O)=C6C7=O)=O)C7=CC=C1
分子式 C32H35NO13 分子量 641.62
溶解度 DMSO: ≥ 100 mg/mL (155.86 mM); Water: < 0.1 mg/mL (insoluble) 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 1.5586 mL 7.7928 mL 15.5855 mL
5 mM 0.3117 mL 1.5586 mL 3.1171 mL
10 mM 0.1559 mL 0.7793 mL 1.5586 mL
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Research Update

Evaluation of PNU-159682 antibody drug conjugates (ADCs)

Bioorg Med Chem Lett 2020 Dec 15;30(24):127640.PMID:33127540DOI:10.1016/j.bmcl.2020.127640.

PNU-159682 is a highly potent secondary metabolite of nemorubicin belonging to the anthracycline class of natural products. Due to its extremely high potency and only partially understood mechanism of action, it was deemed an interesting starting point for the development of a new suite of linker drugs for antibody drug conjugates (ADCs). Structure activity relationships were explored on the small molecule which led to six linker drugs being developed for conjugation to antibodies. Herein we describe the synthesis of novel PNU-159682 derivatives and the subsequent linker drugs as well as the corresponding biological evaluations of the small molecules and ADCs.

Virtual Cross-Linking of the Active Nemorubicin Metabolite PNU-159682 to Double-Stranded DNA

Chem Res Toxicol 2017 Feb 20;30(2):614-624.PMID:28068470DOI:10.1021/acs.chemrestox.6b00362.

The DNA alkylating mechanism of PNU-159682 (PNU), a highly potent metabolite of the anthracycline nemorubicin, was investigated by gel-electrophoretic, HPLC-UV, and micro-HPLC/mass spectrometry (MS) measurements. PNU quickly reacted with double-stranded oligonucleotides, but not with single-stranded sequences, to form covalent adducts which were detectable by denaturing polyacrylamide gel electrophoresis (DPAGE). Ion-pair reverse-phase HPLC-UV analysis on CG rich duplex sequences having a 5'-CCCGGG-3' central core showed the formation of two types of adducts with PNU, which were stable and could be characterized by micro-HPLC/MS. The first type contained one alkylated species (and possibly one reversibly bound species), and the second contained two alkylated species per duplex DNA. The covalent adducts were found to produce effective bridging of DNA complementary strands through the formation of virtual cross-links reminiscent of those produced by classical anthracyclines in the presence of formaldehyde. Furthermore, the absence of reactivity of PNU with CG-rich sequence containing a TA core (CGTACG), and the minor reactivity between PNU and CGC sequences (TACGCG·CGCGTA) pointed out the importance of guanine sequence context in modulating DNA alkylation.

Formation and antitumor activity of PNU-159682, a major metabolite of nemorubicin in human liver microsomes

Clin Cancer Res 2005 Feb 15;11(4):1608-17.PMID:15746066DOI:10.1158/1078-0432.CCR-04-1845.

Purpose: Nemorubicin (3'-deamino-3'-[2''(S)-methoxy-4''-morpholinyl]doxorubicin; MMDX) is an investigational drug currently in phase II/III clinical testing in hepatocellular carcinoma. A bioactivation product of MMDX, 3'-deamino-3'',4'-anhydro-[2''(S)-methoxy-3''(R)-oxy-4''-morpholinyl]doxorubicin (PNU-159682), has been recently identified in an incubate of the drug with NADPH-supplemented rat liver microsomes. The aims of this study were to obtain information about MMDX biotransformation to PNU-159682 in humans, and to explore the antitumor activity of PNU-159682. Experimental design: Human liver microsomes (HLM) and microsomes from genetically engineered cell lines expressing individual human cytochrome P450s (CYP) were used to study MMDX biotransformation. We also examined the cytotoxicity and antitumor activity of PNU-159682 using a panel of in vitro-cultured human tumor cell lines and tumor-bearing mice, respectively. Results: HLMs converted MMDX to a major metabolite, whose retention time in liquid chromatography and ion fragmentation in tandem mass spectrometry were identical to those of synthetic PNU-159682. In a bank of HLMs from 10 donors, rates of PNU-159682 formation correlated significantly with three distinct CYP3A-mediated activities. Troleandomycin and ketoconazole, both inhibitors of CYP3A, markedly reduced PNU-159682 formation by HLMs; the reaction was also concentration-dependently inhibited by a monoclonal antibody to CYP3A4/5. Of the 10 cDNA-expressed CYPs examined, only CYP3A4 formed PNU-159682. In addition, PNU-159682 was remarkably more cytotoxic than MMDX and doxorubicin in vitro, and was effective in the two in vivo tumor models tested, i.e., disseminated murine L1210 leukemia and MX-1 human mammary carcinoma xenografts. Conclusions: CYP3A4, the major CYP in human liver, converts MMDX to a more cytotoxic metabolite, PNU-159682, which retains antitumor activity in vivo.

The interaction of nemorubicin metabolite PNU-159682 with DNA fragments d(CGTACG)(2), d(CGATCG)(2) and d(CGCGCG)(2) shows a strong but reversible binding to G:C base pairs

Bioorg Med Chem 2012 Dec 15;20(24):6979-88.PMID:23154079DOI:10.1016/j.bmc.2012.10.033.

The antitumor anthracycline nemorubicin is converted by human liver microsomes to a major metabolite, PNU-159682 (PNU), which was found to be much more potent than its parent drug toward cultured tumor cells and in vivo tumor models. The mechanism of action of nemorubicin appears different from other anthracyclines and until now is the object of studies. In fact PNU is deemed to play a dominant, but still unclear, role in the in vivo antitumor activity of nemorubicin. The interaction of PNU with the oligonucleotides d(CGTACG)(2), d(CGATCG)(2) and d(CGCGCG)(2) was studied with a combined use of (1)H and (31)P NMR spectroscopy and by ESI-mass experiments. The NMR studies allowed to establish that the intercalation between the base pairs of the duplex leads to very stable complexes and at the same time to exclude the formation of covalent bonds. Melting experiments monitored by NMR, allowed to observe with high accuracy the behaviour of the imine protons with temperature, and the results showed that the re-annealing occurs after melting. The formation of reversible complexes was confirmed by HPLC-tandem mass spectra, also combined with endonuclease P1digestion. The MS/MS spectra showed the loss of neutral PNU before breaking the double helix, a behaviour typical of intercalators. After digestion with the enzyme, the spectra did not show any compound with PNU bound to the bases. The evidence of a reversible process appears from both proton and phosphorus NOESY spectra of PNU bound to d(CGTACG)(2) and to d(CGATCG)(2). The dissociation rate constants (k(off)) of the slow step of the intercalation process, measured by (31)P NMR NOE-exchange experiments, showed that the kinetics of the process is slower for PNU than for doxorubicin and nemorubicin, leading to a 10- to 20-fold increase of the residence time of PNU into the intercalation sites, with respect to doxorubicin. A relevant number of NOE interactions allowed to derive a model of the complexes in solution from restrained MD calculations. The conformation of PNU bound to the oligonucleotides was also derived from the coupling constant values.

In vitro hepatic conversion of the anticancer agent nemorubicin to its active metabolite PNU-159682 in mice, rats and dogs: a comparison with human liver microsomes

Biochem Pharmacol 2008 Sep 15;76(6):784-95.PMID:18671948DOI:10.1016/j.bcp.2008.07.003.

We recently demonstrated that nemorubicin (MMDX), an investigational antitumor drug, is converted to an active metabolite, PNU-159682, by human liver cytochrome P450 (CYP) 3A4. The objectives of this study were: (1) to investigate MMDX metabolism by liver microsomes from laboratory animals (mice, rats, and dogs of both sexes) to ascertain whether PNU-159682 is also produced in these species, and to identify the CYP form(s) responsible for its formation; (2) to compare the animal metabolism of MMDX with that by human liver microsomes (HLMs), in order to determine which animal species is closest to human beings; (3) to explore whether differences in PNU-159682 formation are responsible for previously reported species- and sex-related differences in MMDX host toxicity. The animal metabolism of MMDX proved to be qualitatively similar to that observed with HLMs since, in all tested species, MMDX was mainly converted to PNU-159682 by a single CYP3A form. However, there were marked quantitative inter- and intra-species differences in kinetic parameters. The mouse and the male rat exhibited V(max) and intrinsic metabolic clearance (CL(int)) values closest to those of human beings, suggesting that these species are the most suitable animal models to investigate MMDX biotransformation. A close inverse correlation was found between MMDX CL(int) and previously reported values of MMDX LD(50) for animals of the species, sex and strain tested here, indicating that differences in the in vivo toxicity of MMDX are most probably due to sex- and species-related differences in the extent of PNU-159682 formation.