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编 号：F761248
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规格
价格
是否有货
1mg
询价
询价
5mg
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询价
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CAS No: 899796-83-9
产品详情
生物活性：
Milatuzumab (hLL1; MEDI-115) is a humanized anti-CD74 monoclonal antibody. CD74, a integral membrane protein, is associated with the promotion of B-cell growth and survival. Milatuzumab causes free radical oxygen generation, and loss of mitochondrial membrane potential. Milatuzumaba also decreases CD20/CD74 aggregates and cell adhesion, to lead to cell death.
体内研究：
Milatuzumaba（15 mg/kg/天；腹腔注射；每 3 天一次）显着提高携带 Jeko 癌细胞的雌性 SCID 小鼠的存活率。并且Milatuzumaba与Rituximab (HY-P9913) 在该小鼠模型中具有协同作用。Animal Model:Jeko mouse model
Dosage:15 mg/kg/day; with or without 15 mg/kg Rituximab
Administration:Intraperitoneal injection; once every 3 days, starting at day 15 after engraftment
Result:Resulted the mean survival for the combination treated group of 44.5 days, compared with 33.5 days for Milatuzumaba treated, 28 days for control.
体外研究：
Milatuzumaba（5 μg/mL；8-48 小时）增强 MCL 细胞系和原发性患者肿瘤细胞的细胞死亡。Milatuzumaba（5 μg/mL；0.5-2 h）在 Jeko、Mino 和 SP-53 细胞中介导细胞毒性，部分取决于 ROS 的产生和线粒体跨膜电位的丧失。Milatuzumaba（5 μg/mL；4 小时）抑制 NF-κB 通路并诱导细胞凋亡，凋亡机制与 caspase 裂解、Bcl-2 家族成员失调或诱导自噬无关。
Milatuzumab (hLL1; MEDI-115) is a humanized anti-CD74 monoclonal antibody. CD74, a integral membrane protein, is associated with the promotion of B-cell growth and survival. Milatuzumab causes free radical oxygen generation, and loss of mitochondrial membrane potential. Milatuzumaba also decreases CD20/CD74 aggregates and cell adhesion, to lead to cell death.
体内研究：
Milatuzumaba（15 mg/kg/天；腹腔注射；每 3 天一次）显着提高携带 Jeko 癌细胞的雌性 SCID 小鼠的存活率。并且Milatuzumaba与Rituximab (HY-P9913) 在该小鼠模型中具有协同作用。Animal Model:Jeko mouse model
Dosage:15 mg/kg/day; with or without 15 mg/kg Rituximab
Administration:Intraperitoneal injection; once every 3 days, starting at day 15 after engraftment
Result:Resulted the mean survival for the combination treated group of 44.5 days, compared with 33.5 days for Milatuzumaba treated, 28 days for control.
体外研究：
Milatuzumaba（5 μg/mL；8-48 小时）增强 MCL 细胞系和原发性患者肿瘤细胞的细胞死亡。Milatuzumaba（5 μg/mL；0.5-2 h）在 Jeko、Mino 和 SP-53 细胞中介导细胞毒性，部分取决于 ROS 的产生和线粒体跨膜电位的丧失。Milatuzumaba（5 μg/mL；4 小时）抑制 NF-κB 通路并诱导细胞凋亡，凋亡机制与 caspase 裂解、Bcl-2 家族成员失调或诱导自噬无关。
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