| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | Mv1Lu and C2C12 cells |
Preparation Method | Cells were pretreated for 1 h with 1uM small molecule inhibitors A 83-01 and then cultured with TGF-β. |
Reaction Conditions | 1uM A-83-01, 1 h |
Applications | The effects of TGF-β inhibitors on cell proliferation were examined. A 83-01 efficiently prevented the growth-inhibitory effects of TGF-β, A-83-01 prevented inhibition of growth of Mv1Lu cells by TGF-β in a dose-dependent fashion. Treatment with 0.3 uM A 83-01 completely blocked the growth-inhibitory effect of TGF-β. |
Animal models | M109 cells were inoculated subcutaneously into CDF1 female mice (5 weeks old) |
Preparation Method | When the tumor volume reached approximately 100-200 mm3, SL, F-SL, or free DXR was injected intravenously at 8 mg/kg, with or without intraperitoneal injection of 0.5 mg A 83-01/kg. The control group was injected intravenously with saline (0.2 mL/20 g body weight) with intraperitoneal injection of the vehicle (0.1 mL/20 g body weight). |
Dosage form | 0.5 mg A-83-01/kg,16day |
Applications | The liposomal DXR injected group showed a strong antitumor effect in comparison with saline with or without A 83-01 and free DXR treated groups. A 83-01 alone did not show an antitumor effect. F-SL with A 83-01 showed a significantly stronger antitumor effect than F-SL alone on day 7 and days 13 and 16, SL alone on day 7 and days 10 and 13, or SL with A 83-01 on days 7 and 10. |
| 产品描述 | A 83-01 is a potent inhibitor of TGF-β type I receptor ALK5 kinase, type I nodal receptor ALK4 and type I nodal receptor ALK7, with IC50s of 12 nM,45 nM and 7.5 nM against the transcription induced by ALK5, ALK4 and ALK7, respectively[1]. A 83-01 reduces the level of ALK-5-induced transcription in Mv1Lu cells, also blocks the ALK4-TD and ALK7-TD induced transcription R4-2 cells, and weakly suppresses that induced by constitutively active ALK-6, ALK-2, ALK-3, and ALK-1. A 83-01 (0.03-10 μM) potently prevents the growth-inhibitory effects of TGF-β, and completely inhibits the effect at 3 μM. A 83-01 (1-10 μM) inhibits TGF-β-induced Smad activation in HaCaT cells[1]. A 83-01 (1 μM) decreases cell motility, adhesion and invasion increased by TGF-β1 in HM-1 cells, but does not change cell proliferation[2]. A-83-01-treated retinal pigment epithelium (RPE) failed to differentiate after 7 passages (P7). Exogenous expression of MYCN and OTX2 in conjunction with A 83-01 restored P7-RPE differentiation to a status similar to minimally passaged RPE[5]. When co-administrated F-SL with A 83-01. Intraperitoneally injected A 83-01-induced alterations in the cancer-associated neovasculature were examined by magnetic resonance imaging (MRI) and histological analysis. The targeting efficacy of single intravenous injections of F-SL combined with A 83-01 was evaluated by measurement of the biodistribution and the antitumor effect in mice bearing murine lung carcinoma M109. A 83-01 temporarily changed the tumor vasculature around 3 h post injection. A 83-01 induced 1.7-fold higher drug accumulation of F-SL in the tumor than liposome alone at 24 h post injection. Moreover F-SL co-administrated with A 83-01 showed significantly greater antitumor activity than F-SL alone[3]. A 83-01 treatment significantly increased the number of Nkx2.5(+) cardiomyoblasts at baseline and after myocardial injury, resulting in an increase in newly formed cardiomyocytes[6]. Using transgenic Nkx2.5 enhancer-green fluorescent protein (GFP) reporter mice, and isolated cardiac progenitor cells (CPC). A 83-01 was found to induce proliferation mainly through increasing Birc5 expression in the MEK/ERK-dependent pathway[7]. Treatment of rat dermal fibroblast with A 83-01 inhibited transforming growth factor-β1 (TGF-β1)-dependent induction of α-SMA and collagen type I[4]. References: |
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