| Description |
BLU2864 is an orally active, highly selective, ATP-competitive PRKACA inhibitor (IC50=0.3 nM). BLU2864 shows anti-tumor activity. BLU2864 can be used in cancer and polycystic kidney disease research[1][2].
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| Related Catalog |
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| Target |
IC50: 0.3 nM (PRKACA)[2]
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| In Vitro |
BLU2864 (40 nM and 200 nM; 5 d) inhibits forskolin (HY-15371)-induced in vitro cystogenesis[1]. Cell Viability Assay[1] Cell Line: mIMCD3 cells Concentration: 40 nM and 200 nM Incubation Time: 5 days Result: Inhibited forskolin induced in vitro cystogenesis of mIMCD3 cells cultured in Matrigel by 72% and 100% at 40 and 200 nM concentrations, respectively, relative to control.
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| In Vivo |
BLU2864 (oral gavage; 45 mg/kg; once daily; 5 d) inhibits renal PKA activity in Pkd1RC/RC mice[1]. BLU2864 (oral gavage; 30 mg/kg; once daily; 5 d) inhibits PKA activity and ameliorates PKD in Pkd1RC/RC mice[1]. BLU2864 (oral gavage; 30 mg/kg and 75 mg/kg; once daily; 34 d) reduces FLC tumor growth in vivo[2]. Animal Model: Pkd1RC/RC mice[1] Dosage: 45 mg/kg Administration: Oral gavage; 45 mg/kg; once daily; 5 days Result: Suppressed kidney basal and total PKA activities by 74% and 87% at 3 hours and by 46% and 56% at 15 hours, respectively, in the BLU2864-treated mice compared with controls. Animal Model: Pkd1RC/RC mice[1] Dosage: 30 mg/kg Administration: Oral gavage; 30 mg/kg; once daily; 5 days Result: Showed higher urine outputs at 15 weeks in the BLU2864-treated mice than in the controls. Showed lower kidney weights, kidney volumes as percent of body weights, and cyst indices. Showed renal basal and total PKA activities by 69% and 84% lower in the BLU2864-treated mice compared with controls. Animal Model: Mice harboring FLC PDX tumors[2] Dosage: 30 mg/kg and 75 mg/kg Administration: Oral gavage; 30 mg/kg and 75 mg/kg; once daily; 34 days Result: Inhibited tumor growth by 48.5% (P=0.003) and by 45.3% (P=0.0005), respectively, at day 34.
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| References |
[1]. Xiaofang Wang, et al. Protein Kinase A Downregulation Delays the Development and Progression of Polycystic Kidney Disease. J Am Soc Nephrol. 2022 Jun;33(6):1087-1104. [2]. Stefanie S. Schalm, et al. Evaluation of PRKACA as a Therapeutic Target for Fibrolamellar Carcinoma. bioRxiv 2022.01.31.477690.
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