1243262-17-0

1243262-17-0 structure
1243262-17-0 structure
  • Name: Demcizumab
  • Chemical Name: Demcizumab
  • CAS Number: 1243262-17-0
  • Molecular Formula:
  • Molecular Weight: 145.65 (kDa)
  • Catalog: Signaling Pathways Stem Cell/Wnt Notch
  • Create Date: 2023-01-18 12:02:54
  • Modify Date: 2024-01-15 19:42:56
  • Demcizumab (OMP 21M18) is an anti-DLL4 monoclonal antibody. Demcizumab is a potent inhibitor of the Notch pathway. Demcizumab alone or in combination with chemotherapy is effective in various cancer models[1][2][3].

Name Demcizumab
Description Demcizumab (OMP 21M18) is an anti-DLL4 monoclonal antibody. Demcizumab is a potent inhibitor of the Notch pathway. Demcizumab alone or in combination with chemotherapy is effective in various cancer models[1][2][3].
Related Catalog
Target

DLL4[1]

In Vitro Demcizumab (0-100 μg/mL) 结合人 DLL4 但不结合鼠 DLL4,并在 FACS 结合测定中阻断 DLL4 与 Notch1 受体的结合[3]。 Demcizumab (20 μg/mL,48 小时) 降低 PDTALL 细胞中的 HES1 和 DTX1 mRNA 表达[4]。 Demcizumab (0-80 μg/mL,1 或 2 或 3 天) 促进 PDTALL13 细胞死亡和早期凋亡[4]。 Cell Viability Assay[4] Cell Line: PDTALL13 (patient-derived T-ALL 13) cell Concentration: 0, 0.5, 1, 5, 10, 20, 40, 80 μg/mL Incubation Time: 1 or 2 or 3 days Result: Dose-dependently inhibited cell viability.
In Vivo Demcizumab (10 mg/kg,i.p.,每周一次) 联合 Irinotecan (7.5 mg/kg) 在 KRASWT 和 KRASMT CRC 异种移植模型中显示出显着的抗肿瘤作用[2]. Demcizumab 单独或与伊立替康 (7.5 mg/kg) 联合使用对 OMP-C8 结肠肿瘤有效[3]。 Demcizumab (20 mg/kg/周,腹腔注射) 增加注射了 PDTALL13 细胞的受辐照 NRG 小鼠的存活率[4]。 Animal Model: KRASWT and KRASMT CRC xenografts[2] Dosage: 10 mg/kg, together with Irinotecan (HY-16562) (7.5 mg/kg) Administration: Intraperitoneal injection (i.p.), once a week Result: Resulted in tumor regression at day 20.
References

[1]. Smith DC, et al. A phase I dose escalation and expansion study of the anticancer stem cell agent demcizumab (anti-DLL4) in patients with previously treated solid tumors. Clin Cancer Res. 2014 Dec 15;20(24):6295-303.  

[2]. Fischer M, et al. Anti-DLL4 inhibits growth and reduces tumor-initiating cell frequency in colorectal tumors with oncogenic KRAS mutations. Cancer Res 2011;71:1520-5.  

[3]. Hoey T, et al. DLL4 blockade inhibits tumor growth and reduces tumor-initiating cell frequency. Cell Stem Cell 2009;5:168–77.  

[4]. Xiong H, et al. Spleen plays a major role in DLL4-driven acute T-cell lymphoblastic leukemia. Theranostics. 2021 Jan 1;11(4):1594-1608.  

Molecular Weight 145.65 (kDa)