| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | AML cells |
Preparation Method | Cells were plated and treated with vehicle DMSO or APTO-253 (LOR-253) (10 concentrations) in 96-well plates for 5 days at 37℃ and 5% CO2. Cell viability was measured using CellTiter 96 AQueous one solution (MTS) cell proliferation assay (Promega, catalog #G3581), and IC50 values were calculated using GraphPad Prism 7 software. |
Reaction Conditions | 10-9-10-4mM APTO-253 (LOR-253) for 5 days |
Applications | APTO-253 (LOR-253) induces cytotoxicity, upregulates p21, and induces G0-G1 cell-cycle arrest in AML cells |
Animal models | DBA/1J male mice (6 weeks) with collagen induced arthritis (CIA) |
Preparation Method | APTO-253 (LOR-253) twice per day for 2 consecutive days per week for 14 days(IV) |
Dosage form | 15 mg/kg APTO-253 (LOR-253) for 14 days |
Applications | APTO-253 (LOR-253) has significant preventive and therapeutic effects on the formation of arthritis. |
| 产品描述 | APTO-253 is a novel small molecule that exerts potent antitumor activity by inducing Kruppel-like factor 4(KLF4) master transcription factor gene expression, thereby inhibiting cell cycle and leading to programmed cell death. APTO-253 (LOR-253)mediates cancer cell resistance by inducing KLF4. APTO-253 (LOR-253) can treat arthritis[2,3]. In p53-mutated TNBC cells, inhibition of KLF4 by RNA interference reduced NOXA expression. Furthermore, treatment of TNBC cells with a KLF4-inducing small compound, APTO-253, resulted in the induction of NOXA expression and NOXA-mediated apoptosis[4]. APTO-253 (LOR-253) inhibited proliferation in AML cell lines and various forms of lymphoma cell lines with IC50 values ranging from 57 nmol/L to 1.75 μmol/L, APTO-253 (LOR-253) induces cytotoxicity, upregulates p21, and induces G0-G1 cell-cycle arrest in AML cells[1].Enforced KLF4 expression by lentiviral transduction sensitized ovarian cancer cells to the effects of the chemotherapy drugs, paclitaxel and cisplatin. Treatment of ovarian cancer cells with APTO-253 (LOR-253) enhanced the efficacy of both chemotherapy drugs. KLF4 expression mediated by lentiviral vector or induced by APTO-253 (LOR-253) resulted in G1 phase arrest in ovarian cancer cells[5]. In mice，APTO-253 (LOR-253) has significant preventive and therapeutic effects on the formation of arthritis[3]. APTO-253 (LOR-253) has antitumor activity in murine xenograft models of the human solid tumors and was advanced into a phase I clinical trial in patients with advanced solid tumors[6]. In that solid tumor clinical trial, APTO-253 (LOR-253) was well tolerated and produced evidence of antitumor activity in patients with advanced refractory solid tumors but did not produce myelosuppression even at the maximum tested dose. The most common treatment-emergent adverse effects of any grade were rash, peripheral neuropathy, hypersensitivity(<10%), and fatigue[7] References: |
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