Dual PARP EGFR ligand for PROTAC Chemical Structure
规格
是否有货
100 mg
询价
250 mg
询价
500 mg
询价
* Please select Quantity before adding items.
生物活性
Dual PARP EGFR ligand for PROTAC incorporates a ligand for PARP and EGFR , and a PROTAC linker, which recruit E3 ligases (such as VHL, CRBN, MDM2, and IAP). Dual PARP EGFR ligand for PROTAC can be used in the synthesis of DP-C-4, which is CRBN-based dual PROTAC for simultaneous degradation of EGFR and PARP[1].
分子量
1020.52
Formula
C53H56ClF2N9O8
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Mengzhu Zheng, et al. Rational Design and Synthesis of Novel Dual PROTACs for Simultaneous Degradation of EGFR and PARP. J Med Chem. 2021 May 26.
PARP1-IN-5 is a low toxicity, orally active, potent and selective PARP-1 inhibitor (IC50 =14.7 nM). PARP1-IN-5 can be used for the research of cancer[1].
IC50 & Target[1]
PARP-1
14.7 nM (IC50)
PARP-2
0.9 μM (IC50)
体外研究 (In Vitro)
PARP1-IN-5 (0.1~10 μM; A549 cells) can significantly increase the cytotoxicity of CBP on A549 cells in a dose-dependent manner. PARP1-IN-5 (0.1~10 μM; SK-OV-3 cells) decreases the expressions of MCM2-7. PARP1-IN-5 (0.1~320 μM; A549 cells) has little cytotoxic effects on A549 cells. PARP1-IN-5 (SK-OV-3 cells) can significantly decrease the PAR level[1]. PARP1-IN-5 exerts antitumor effects through PARP-1. PARP1-IN-5 could increase the γ-H2AX expression[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
PARP1-IN-5 (1000 mg/kg; p.o.) shows that there is no significant difference in the body weight and blood routine[1]. PARP1-IN-5 (25 and 50 mg/kg; p.o.; 12 days) significantly enhances the inhibitory effect of carboplatin on A549 cells at 50 mg/kg[1]. PARP1-IN-5 (50 mg/kg; p.o.) positively correlates with the expression of PARP-1[1]. PARP1-IN-5 can upregulate the expression of γ-H2AX and decrease the expression of PAR[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Mice[1]
Dosage:
1000 mg/kg
Administration:
P.o.
Result:
There was no significant difference in the body weight and blood routine.
Animal Model:
Mice[1]
Dosage:
25 and 50 mg/kg
Administration:
P.o.; 12 days
Result:
Significantly enhanced the inhibitory effect of CBP on A549 cells at 50 mg/kg.
Animal Model:
Male Sprague−Dawley (SD) rats[1]
Dosage:
50 mg/kg (Pharmacokinetic Analysis)
Administration:
P.o.; 12 days
Result:
Positively correlated with the expression of PARP-1.
分子量
464.53
Formula
C25H24N2O5S
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Long H, et al. Discovery of Novel Apigenin-Piperazine Hybrids as Potent and Selective Poly (ADP-Ribose) Polymerase-1 (PARP-1) Inhibitors for the Treatment of Cancer. J Med Chem. 2021;64(16):12089-12108.
E7449 is a potent PARP1 and PARP2 inhibitor and also inhibits TNKS1 and TNKS2, with IC50s of 2.0, 1.0, ∼50 and ∼50 nM for PARP1, PARP2, TNKS1 and TNKS2, respectively, using 32P-NAD+ as substrate.
IC50 & Target[1]
PARP2
1 nM (IC50)
PARP1
2 nM (IC50)
TNKS1
50 nM (IC50)
TNKS2
50 nM (IC50)
体外研究 (In Vitro)
E7449 is a potent PARP1 and PARP2 inhibitor and also inhibits TNKS1 and TNKS2, with IC50s of 2.0, 1.0, ∼50 and ∼50 nM for PARP1, PARP2, TNKS1 and TNKS2, respectively, using 32P-NAD+ as substrate. E7449 shows no obvious inhibiotry effects on PARP3 or PARPs 6-16. E7449 traps PARP1 onto damaged DNA, and affects DNA repair pathways beyond homologous recombination (HR). E7449 most potnetly suppresses cells deficient in components of the HR pathway (BRCA1 and 2, CtIP, Rad54). E7449 (10 μM) inhibits Wnt signaling in SW480 cells[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
E7449 moderately inhibits the growth of tumors at 100 mg/kg, and significantly ehhances the inhibition via 10, 30 and 100 mg/kg oral dosing in combination with temozolomide (TMZ) in the mouse melanoma B16-F10 isograft model. E7449 (30 or 100 mg/kg, p.o.) inhibits PARP, shows anti-tumor activity, and is well-tolerated without any obvious body weight loss or deaths in a BRCA mutant xenograft model. E7449 (30, 100 or 300 mg/kg, p.o.) suppresses re-growth of hair in a dose dependent manner, and blocks Wnt signaling in C57BL/6 mice. E7449 (100 mg/kg, p.o.) combined with MEK inhibitor exhibits antitumor activity in a Wnt1 subcutaneous model (mammary tumors initially isolated from Wnt1 (int-1) transgenic mice)[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
317.34
Formula
C18H15N5O
CAS 号
1140964-99-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Powder
-20°C
3 years
4°C
2 years
In solvent
-80°C
6 months
-20°C
1 month
溶解性数据
In Vitro:
DMSO : 6.4 mg/mL (20.17 mM; Need ultrasonic and warming)
[1]. McGonigle S, et al. E7449: A dual inhibitor of PARP1/2 and tankyrase1/2 inhibits growth of DNA repair deficient tumors and antagonizes Wnt signaling. Oncotarget. 2015 Dec 1;6(38):41307-23.
Kinase Assay [1]
Briefly, 24 to 48 h after transfection, cells are washed 3× in ice-cold PBS and lysed for 20 min on ice in cell lysis buffer (CLB: 50 mM HEPES, pH 7.4, 150 mM NaCl, 1 mM MgCl2, 1 mM EGTA, 1 mM DTT, 1% TritonX-100, 1 μg/mL leupeptin, aprotinin, pepstatin, PMSF). Lysates are subject to ultracentrifugation at 100,000 g for 30 min. Cleared lysates are incubated for 1 h at 4°C with anti-GFP antibody (3E6) and pre-bound protein A magnetic beads. Beads are then washed 1 × 5 min in CLB, followed by 3 × 10 min washes in CLB containing 1 M NaCl, and 1 × 5 min wash in PARP reaction buffer (PRB; 50 mM Tris, pH 7.5, 50 mM NaCl, 0.5 mM DTT, 0.1% TritonX-100, 1 μg/mL leupeptin, aprotinin, pepstatin). NAD+ incorporation reactions are performed in PRB containing 10 μM NAD+ supplemented with 32P-NAD+ at 1:20 ratio for 30 min at 25°C. For PARPs with low incorporation signals (PARP4, 5a and 16), NAD+ incorporation is performed at 1:5 ratio for 1 h at 25°C. Beads are then re-suspended in Laemmli sample buffer, heated to 65°C for 10 min, the beads removed using a magnet, and the supernatant spotted onto Whatman paper. Samples are analyzed via phosphorimaging[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
Proliferation assays are performed in a panel of 32 isogenic DT40 cell lines, in which each line is deficient in a distinct DNA repair gene. Cells are seeded and incubated with test compound at various concentrations for 2-3 days (∼ 8 cell cycles). Cell growth is assessed using XTT and IC50 values are calculated using the GraphPad Prism 5 software version 5.02. Each experiment is conducted in duplicate and a minimum of 3 separate experiments are performed. Human breast cancer cell lines, HCC1143, HCC70, HCC1806, MDA-MB-436, T47D, MDA-MB-157, MDA-MB-231, MDA-MB-468, MDA-MB-453, BT-20 and Hs578T are used. For cell line panel assays, cells are maintained and assayed in RPMI 1640 or DMEM medium containing 10% FBS. For proliferation assays cells are plated at low density in 96 well plates. E7449 is added at various concentrations and plates incubated for a total of 8 days; compound and medium are replenished on day 4. Cell growth is assessed using the CellTiter-Glo cell viability assay. Each experiment is conducted in duplicate and a minimum of 3 separate experiments are performed[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1]
Temozolomide (TMZ) combination in B16-F10 isograft model: female C57BL/6 mice are inoculated subcutaneously with B16-F10 cells (2 × 105). Following randomization by body weight, drug treatment is initiated 1 day post-inoculation. Both E7449 and TMZ are formulated in 0.5% methyl cellulose and orally administrated once per day. TMZ is administered daily on days 1 to 5 at 50 mg/kg as a single agent or in combination. E7449 is administered daily on days 1 to 7 at doses of 10, 30 and 100 mg/kg in combination with TMZ and at a dose of 100 mg/kg as a single agent. The control group is treated with vehicle (0.5% methyl cellulose in water). E7449 or vehicle is administered first and when dosing of all animals is complete TMZ is administered to animals receiving the combination[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. McGonigle S, et al. E7449: A dual inhibitor of PARP1/2 and tankyrase1/2 inhibits growth of DNA repair deficient tumors and antagonizes Wnt signaling. Oncotarget. 2015 Dec 1;6(38):41307-23.
PARP1-IN-7 is an inhibitor of poly(ADP-ribose) polymerase-1 (PARP1) as an anticancer agent.
分子量
397.47
Formula
C24H23N5O
CAS 号
2084112-75-2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Karche NP, et al. Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization. Bioorg Med Chem. 2020 Dec 15;28(24):115819.
UPF 1069 is a PARP inhibitor, with IC50s of 8 and 0.3 μM for PARP-1 and PARP-2, respectively.
IC50 & Target[1][2]
PARP-2
0.3 μM (IC50)
PARP-1
8 μM (IC50)
体外研究 (In Vitro)
UPF 1069 (Compound 55) is a PARP inhibitor, with IC50s of 8 and 0.3 μM for PARP-1 and PARP-2, respectively[1]. UPF 1069 (1 µM) reduces the residual PARP activity by approximately 80% of PARP-1-deficient fibroblasts, but only slightly inhibits the enzymic activity in wild-type fibroblasts. UPF 1069 (0.1-1 µM) markedly enhances CA1 hippocampal damage. UPF 1069 (10 µM) also exacerbates oxygen-glucose deprivation (OGD) damage in organotypic hippocampal slices. However, UPF 1069 alleviates the damage cuased by OGD in mixed cortical cell cultures, shows a potent neuroprotective activity both at a concentration (1 µM) selectively acting on PARP-2 and at a concentration (10 µM) inhibiting both PARP-1 and PARP-2 activities[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
279.29
Formula
C17H13NO3
CAS 号
1048371-03-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Pellicciari R, et al. On the way to selective PARP-2 inhibitors. Design, synthesis, and preliminary evaluation of a series of isoquinolinone derivatives. ChemMedChem. 2008 Jun;3(6):914-23.
[2]. Moroni F, et al. Selective PARP-2 inhibitors increase apoptosis in hippocampal slices but protect cortical cells in models of post-ischaemic brain damage.
Kinase Assay [2]
PARP activity is evaluated by utilizing commercially available recombinant bovine PARP-1 and mouse PARP-2. Briefly, the enzymatic reaction is carried out in 100 µL of 50 mM Tris-HCl (pH 8.0) containing 5 mM MgCl2, 2 mM dithiothreitol, 10 µg sonicated calf thymus DNA, 0.2 µCi [adenine-2,8-3H]NAD and recombinant enzyme PARP-1 or PARP-2 (0.03 U per sample). Different concentrations of the putative inhibitors are added, and the mixture is incubated for 1 h at 37°C. The reaction is terminated by adding 1 mL of 10% trichloroacetic acid (w/v) and centrifuged. Pellets are then washed twice with 1 mL of H2O and resuspended in 1 mL of 0.1 M NaOH. The radioactivity incorporated from [adenine-2,8-3H]NAD into proteins is evaluated by liquid scintillation spectrometry[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Pellicciari R, et al. On the way to selective PARP-2 inhibitors. Design, synthesis, and preliminary evaluation of a series of isoquinolinone derivatives. ChemMedChem. 2008 Jun;3(6):914-23.
[2]. Moroni F, et al. Selective PARP-2 inhibitors increase apoptosis in hippocampal slices but protect cortical cells in models of post-ischaemic brain damage.
Rucaparib (AG014699) monocamsylate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib monocamsylate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib monocamsylate has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target[1][4]
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) monocamsylate is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) monocamsylate is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib monocamsylate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib monocamsylate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib monocamsylate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) monocamsylate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) monocamsylate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) monocamsylate results in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) monocamsylate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) monocamsylate has greatest antitumor effect with three complete regressions[2]. Rucaparib monocamsylate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female CD-1 nude mice aged 10-12 weeks with Capan-1 cells[2]
Dosage:
10 mg/kg or 50, 150 mg/kg
Administration:
10 mg/kg for i.p. or 50, 150 mg/kg for p.o.
Result:
Significantly inhibited the growth of the tumor.
Clinical Trial
分子量
555.66
Formula
C29H34FN3O5S
CAS 号
1859053-21-6
中文名称
瑞卡帕布樟脑磺酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
3-Aminobenzamide (PARP-IN-1) is a potent inhibitor of PARP with IC50 of appr 50 nM in CHO cells, and acts as a mediator of oxidant-induced myocyte dysfunction during reperfusion.
IC50 & Target[1]
PARP
50 nM (IC50)
体外研究 (In Vitro)
3-Aminobenzamide (PARP-IN-1) (>1 μM) causes more than 95% inhibition of PARP activity without significant cellular toxicity. INO-1001 significantly sensitizes CHO cells by blocking most of the DNA repair occurring between radiation fractions[1]. 3-Aminobenzamide significantly improves endothelial function by enhancing the acetylcholine-induced, endothelium-dependent, nitric oxide mediated vasorelaxation after exposure with 400 μM H2O2[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
In a db/db (Leprdb/db) mouse model, 3-Aminobenzamide ameliorates diabetes-induced albumin excretion and mesangial expansion, and also decreases diabetes-induced podocyte depletion[3]. 3-Aminobenzamide (1.6 mg/kg via intracerebral injection) prevents NAD+ depletion and improves water maze performance after controlled cortical impact (CCI) in mice[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
136.15
Formula
C7H8N2O
CAS 号
3544-24-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Brock WA, et al. Radiosensitization of human and rodent cell lines by INO-1001, a novel inhibitor of poly(ADP-ribose) polymerase. Cancer Lett. 2004 Mar 18;205(2):155-60.
[2]. Radovits T, et al. Poly(ADP-ribose) polymerase inhibition improves endothelial dysfunction induced by reactive oxidant hydrogen peroxide in vitro. Eur J Pharmacol. 2007 Jun 14;564(1-3):158-66.
[3]. Szabo C, et al. Poly(ADP-ribose) polymerase inhibitors ameliorate nephropathy of type 2 diabetic Leprdb/db mice. Diabetes. 2006 Nov;55(11):3004-12.
[4]. Clark RS, et al. Local administration of the poly(ADP-ribose) polymerase inhibitor INO-1001 prevents NAD+ depletion and improves water maze performance after traumatic brain injury in mice. J Neurotrauma. 2007 Aug;24(8):1399-405.
Kinase Assay [1]
PARP activity is measured with a PARP Activity Assay Kit. This method measures relative PARP activity by determining the level of incorporation of 3H-NAD into trichloroacetic acid (TCA) precipitable material in the presence of sheared genomic DNA, which activates PARP. The reaction mixture is added directly to washed cultures in 12-well culture plates and the reaction is allowed to proceed for 60 minutes at 37°C before the cells are removed mechanically, transferred to a microcentrifuge tube, and precipitated with ice-cold 5% TCA.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [3]
Male db/db (Leprdb/db) mice, together with nondiabetic control db/m mice on C57BLKs/J background, are used. INO-1001 and PJ-34 treatment are initiated at 5 weeks of age. In sterile water that is sweetened with NutraSweet, 4.8 g/L 3-Aminobenzamide and 2.4 g/L PJ-34 is dissolved. Control animals receive sweetened water only. The average inhibitor consumption is 60 mg/kg 3-Aminobenzamide and 30 mg/kg PJ-34.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Brock WA, et al. Radiosensitization of human and rodent cell lines by INO-1001, a novel inhibitor of poly(ADP-ribose) polymerase. Cancer Lett. 2004 Mar 18;205(2):155-60.
[2]. Radovits T, et al. Poly(ADP-ribose) polymerase inhibition improves endothelial dysfunction induced by reactive oxidant hydrogen peroxide in vitro. Eur J Pharmacol. 2007 Jun 14;564(1-3):158-66.
[3]. Szabo C, et al. Poly(ADP-ribose) polymerase inhibitors ameliorate nephropathy of type 2 diabetic Leprdb/db mice. Diabetes. 2006 Nov;55(11):3004-12.
[4]. Clark RS, et al. Local administration of the poly(ADP-ribose) polymerase inhibitor INO-1001 prevents NAD+ depletion and improves water maze performance after traumatic brain injury in mice. J Neurotrauma. 2007 Aug;24(8):1399-405.
Rucaparib (AG014699) phosphate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib phosphate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib phosphate has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target[1][2]
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) phosphate is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) phosphate is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib phosphate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib phosphate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib phosphate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) phosphate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) phosphate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) phosphate results in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) phosphate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) phosphate has greatest antitumor effect with three complete regressions[2]. Rucaparib phosphate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female CD-1 nude mice aged 10-12 weeks with Capan-1 cells[1]
Dosage:
10 mg/kg for i.p. or 50, 150 mg/kg for p.o.
Administration:
IP or PO
Result:
Significantly inhibited the growth of the tumor.
Clinical Trial
分子量
421.36
Formula
C19H21FN3O5P
CAS 号
459868-92-9
中文名称
瑞卡帕布磷酸盐;鲁卡帕尼磷酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
Rucaparib (AG014699) phosphate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib phosphate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib phosphate has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target[1][2]
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) phosphate is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) phosphate is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib phosphate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib phosphate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib phosphate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) phosphate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) phosphate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) phosphate results in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) phosphate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) phosphate has greatest antitumor effect with three complete regressions[2]. Rucaparib phosphate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female CD-1 nude mice aged 10-12 weeks with Capan-1 cells[1]
Dosage:
10 mg/kg for i.p. or 50, 150 mg/kg for p.o.
Administration:
IP or PO
Result:
Significantly inhibited the growth of the tumor.
Clinical Trial
分子量
421.36
Formula
C19H21FN3O5P
CAS 号
459868-92-9
中文名称
瑞卡帕布磷酸盐;鲁卡帕尼磷酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
PARP14 inhibitor H10, compound H 10, is a selective inhibitor against PARP14 (IC50=490 nM), over other PARPs (≈24 fold over PARP1). PARP14 inhibitor H10 induces caspase-3/7-mediated cell apoptosis[1].
IC50 & Target
PARP14
490 nM (IC50)
PARP1
分子量
557.58
Formula
C24H27N7O7S
CAS 号
2084811-68-5
运输条件
Room temperature in continental US; may vary elsewhere.
BYK204165 is a potent and selective PARP1 inhibitor. BYK204165 inhibits cell-free recombinant human PARP-1 (hPARP-1) with a pIC50 of 7.35 (pKi=7.05), and murine PARP-2 (mPARP-2) with a pIC50 of 5.38, respectively. BYK204165 displays 100-fold selectivity for PARP-1[1].
IC50 & Target[1]
hPARP-1
7.35 (pIC50)
mPARP-2
5.38 (pIC50)
体外研究 (In Vitro)
In kinetic experiments with human PARP-1, BYK204165 exhibits potent and competitive inhibition of enzyme activity, yielding a pKi value of 7.05[1]. BYK204165 exhibits low potency of PARP inhibition in C4I cells (pIC50 of 5.75)[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
BYK204165 is not investigated in vivo because of its short half-time (t1/2) of 23 min measured at rat microsomes in vitro[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
252.27
Formula
C15H12N2O2
CAS 号
1104546-89-5
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Eltze T, et al. Imidazoquinolinone, imidazopyridine, and isoquinolindione derivatives as novel and potent inhibitors of the poly(ADP-ribose) polymerase (PARP): a comparison with standard PARP inhibitors. Mol Pharmacol. 2008 Dec;74(6):1587-98.
PARP1-IN-5 dihydrochloride is a low toxicity, orally active, potent and selective PARP-1 inhibitor (IC50 =14.7 nM). PARP1-IN-5 dihydrochloride can be used for the research of cancer[1].
IC50 & Target[1]
PARP-1
14.7 nM (IC50)
PARP-2
0.9 μM (IC50)
体外研究 (In Vitro)
PARP1-IN-5 dihydrochloride (0.1~10 μM; A549 cells) can significantly increase the cytotoxicity of CBP on A549 cells in a dose-dependent manner. PARP1-IN-5 dihydrochloride (0.1~10 μM; SK-OV-3 cells) decreases the expressions of MCM2-7. PARP1-IN-5 dihydrochloride (0.1~320 μM; A549 cells) has little cytotoxic effects on A549 cells. PARP1-IN-5 dihydrochloride (SK-OV-3 cells) can significantly decrease the PAR level[1]. PARP1-IN-5 dihydrochloride exerts antitumor effects through PARP-1. PARP1-IN-5 dihydrochloride could increase the γ-H2AX expression[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
PARP1-IN-5 dihydrochloride (1000 mg/kg; p.o.) shows that there is no significant difference in the body weight and blood routine[1]. PARP1-IN-5 dihydrochloride (25 and 50 mg/kg; p.o.; 12 days) significantly enhances the inhibitory effect of carboplatin on A549 cells at 50 mg/kg[1]. PARP1-IN-5 dihydrochloride (50 mg/kg; p.o.) positively correlates with the expression of PARP-1[1]. PARP1-IN-5 dihydrochloride can upregulate the expression of γ-H2AX and decrease the expression of PAR[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Mice[1]
Dosage:
1000 mg/kg
Administration:
P.o.
Result:
There was no significant difference in the body weight and blood routine.
Animal Model:
Mice[1]
Dosage:
25 and 50 mg/kg
Administration:
P.o.; 12 days
Result:
Significantly enhanced the inhibitory effect of CBP on A549 cells at 50 mg/kg.
Animal Model:
Male Sprague−Dawley (SD) rats[1]
Dosage:
50 mg/kg (Pharmacokinetic Analysis)
Administration:
P.o.
Result:
Positively correlated with the expression of PARP-1.
分子量
537.46
Formula
C25H26Cl2N2O5S
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Long H, et al. Discovery of Novel Apigenin-Piperazine Hybrids as Potent and Selective Poly (ADP-Ribose) Polymerase-1 (PARP-1) Inhibitors for the Treatment of Cancer. J Med Chem. 2021;64(16):12089-12108.
Rucaparib (AG014699) hydrochloride is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib hydrochloride is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib hydrochloride has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) hydrochloride is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) hydrochloride is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib hydrochloride is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib hydrochloride can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib hydrochloride inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) hydrochloride and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) hydrochloride significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) hydrochloride results in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) hydrochloride significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) hydrochloride has greatest antitumor effect with three complete regressions[2]. Rucaparib hydrochloride enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
359.83
Formula
C19H19ClFN3O
CAS 号
773059-19-1
中文名称
瑞卡帕布盐酸盐;鲁卡帕尼盐酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
Rucaparib (AG014699) tartrate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib tartrate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib tartrate has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target[1]
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) tartrate is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) tartrate is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib tartrate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib tartrate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib tartrate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) tartrate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) tartrate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) tartrate esults in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) tartrate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) tartrate has greatest antitumor effect with three complete regressions[2]. Rucaparib tartrate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
473.45
Formula
C23H24FN3O7
CAS 号
773059-22-6
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
Rucaparib (AG014699) camsylate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib camsylate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib camsylate has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) camsylate is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) camsylate is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib camsylate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib camsylate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib camsylate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) camsylate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) camsylate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) camsylate results in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) camsylate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) camsylate has greatest antitumor effect with three complete regressions[2]. Rucaparib camsylate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female CD-1 nude mice aged 10-12 weeks with Capan-1 cells[2]
Dosage:
10 mg/kg or 50, 150 mg/kg
Administration:
10 mg/kg for i.p. or 50, 150 mg/kg for p.o.
Result:
Significantly inhibited the growth of the tumor.
Formula
C19H18FN3O.xC10H16O4S
CAS 号
1327258-57-0
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
Rucaparib (AG014699) acetate is an orally active, potent inhibitor of PARP proteins (PARP-1, PARP-2 and PARP-3) with a Ki of 1.4 nM for PARP1. Rucaparib acetate is a modest hexose-6-phosphate dehydrogenase (H6PD) inhibitor. Rucaparib acetate has the potential for castration-resistant prostate cancer (CRPC) research[1][2][3][4].
IC50 & Target[1]
PARP-1
1.4 nM (Ki)
PARP-2
PARP-3
体外研究 (In Vitro)
Rucaparib (AG014699) acetate is a possible N-demethylation metabolite of AG14644[1]. Rucaparib (0.1, 1, 10, 100 μM; 24 hours) acetate is cytotoxic and has the LC50 being 5 μM in Capan-1 (BRCA2 mutant) cells and only 100 nM in MX-1 (BRCA1 mutant) cells[2]. The radio-sensitization by Rucaparib acetate is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib acetate can target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions[5]. Rucaparib acetate inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Rucaparib (AG014699) acetate and AG14584 significantly increase Temozolomide toxicity. Rucaparib (1 mg/kg) acetate significantly increases Temozolomide-induced body weight loss. Rucaparib (0.1 mg/kg) acetate esults in a 50% increase in the temozolomide-induced tumor growth delay[1]. Rucaparib (10 mg/kg for i.p. or 50, 150 mg/kg for p.o.; daily for 5 days per week for 6 weeks) acetate significantly inhibits the growth of the tumor, and there is one complete tumor regression and two persistent partial regressions[2]. Rucaparib (150 mg/kg; p.o.; once per week for 6 weeks or three times per week for 6 weeks) acetate has greatest antitumor effect with three complete regressions[2]. Rucaparib acetate enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
383.42
Formula
C21H22FN3O3
CAS 号
773059-23-7
中文名称
瑞卡帕布醋酸盐;鲁卡帕尼醋酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Thomas HD, et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther, 2007, 6(3), 945-956.
[2]. J Murray, et al. Tumour cell retention of rucaparib, sustained PARP inhibition and efficacy of weekly as well as daily schedules. Br J Cancer. 2014 Apr 15;110(8):1977-84.
[3]. Matt Shirley, et al. Rucaparib: A Review in Ovarian Cancer. Target Oncol. 2019 Apr;14(2):237-246.
[4]. Jianneng Li, et al. Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation. Sci Transl Med. 2021 May 26;13(595):eabe8226.
[5]. Hunter JE, et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699. Oncogene, 2012, 31(2), 251-264.
[6]. Daniel RA, et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res, 2009, 15(4), 1241-1249.
PROTAC PARP1 degrader is a PARP1 degrader based on MDM2 E3 ligand. It induces significant PARP1 cleavage and programmed cell death. PROTAC PARP1 degrader at 10 μM at 24 h inhibits MDA-MB-231 cell line with an IC50 of 6.12 μM.
IC50 & Target[1]
PARP1
MDM2
分子量
1145.09
Formula
C58H63Cl2N11O10
CAS 号
2369022-68-2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Zhao Q, et al. Induction of apoptosis in MDA-MB-231 breast cancer cells by a PARP1-targeting PROTAC small molecule. Chem Commun (Camb). 2019 Jan 2;55(3):369-372.
PARP1-IN-8 (compound 11c) is a potent and BBB-penetrated PARP1 inhibitor, with an IC50 of 97 nM. PARP1-IN-8 shows significantly potent anti-proliferative activity against Human lung adenocarcinoma epithelial cell line A549[1].
[1]. Almahli H, Hadchity E, Jaballah MY, Daher R, Ghabbour HA, Kabil MM, Al-Shakliah NS, Eldehna WM. Development of novel synthesized phthalazinone-based PARP-1 inhibitors with apoptosis inducing mechanism in lung cancer. Bioorg Chem. 2018 Apr;77:443-456.
PARP/EZH2-IN-1 is a first-in-class dual PARP (IC50 6.87 nM) and EZH2 (IC50 36.51 nM) inhibitor for triple-negative breast cancer with wild-type BRCA.
IC50 & Target
PARP-1
6.87 nM (IC50)
EZH2
36.51 nM (IC50)
分子量
768.83
Formula
C43H41FN8O5
CAS 号
2687273-52-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Wang C, et al. Discovery of First-in-Class Dual PARP and EZH2 Inhibitors for Triple-Negative Breast Cancer with Wild-Type BRCA. J Med Chem. 2021 Sep 9;64(17):12630-12650.
PARP/EZH2-IN-1 is a first-in-class dual PARP (IC50 6.87 nM) and EZH2 (IC50 36.51 nM) inhibitor for triple-negative breast cancer with wild-type BRCA.
IC50 & Target
PARP-1
6.87 nM (IC50)
EZH2
36.51 nM (IC50)
分子量
768.83
Formula
C43H41FN8O5
CAS 号
2687273-52-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Wang C, et al. Discovery of First-in-Class Dual PARP and EZH2 Inhibitors for Triple-Negative Breast Cancer with Wild-Type BRCA. J Med Chem. 2021 Sep 9;64(17):12630-12650.