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Cetuximab/西妥昔单抗 {[allProObj[0].p_purity_real_show]}

货号:A879617 同义名: C225

Cetuximab是一种嵌合IgG1单克隆抗体,通过与EGFR胞外结构域结合来阻止其与配体结合。Cetuximab具有用于头颈部鳞状细胞癌和结直肠癌研究的潜力。

Cetuximab/西妥昔单抗 化学结构 CAS号:205923-56-4
Cetuximab/西妥昔单抗 化学结构
CAS号:205923-56-4
Cetuximab/西妥昔单抗 3D分子结构
CAS号:205923-56-4
Cetuximab/西妥昔单抗 化学结构 CAS号:205923-56-4
Cetuximab/西妥昔单抗 3D分子结构 CAS号:205923-56-4
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Cetuximab/西妥昔单抗 纯度/质量文件 产品仅供科研

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产品名称 EGFR/ErbB1 ErbB3 ErbB4 HER2/ErbB2 mutant EGFR 其他靶点 纯度
WZ-3146 ++++

EGFR (E746_A750), IC50: 2 nM

EGFR (E746_A750/T790M), IC50: 14 nM

99%+
Daphnetin +

EGFR, IC50: 7.67 μM

PKA,PKC 95%
Lifirafenib ++

EGFR, IC50: 29 nM

+

EGFR(T790M/L858R), IC50: 495 nM

98%
PD168393 ++++

EGFR, IC50: 0.70 nM

99%+
Nazartinib ++

mutant EGFR, Ki: 0.031 μM

++

mutant EGFR, Ki: 0.031 μM

98%
Norcantharidin 98%
CL-387785 ++++

EGFR, IC50: 370 pM

98%
WHI-P154 +++

EGFR, IC50: 4 nM

Src,VEGFR 98%
Tyrphostin A9 +

EGFR, IC50: 460 μM

PDGFR 98%
AG 555 +

EGFR, IC50: 0.7 μM

98%
AG 494 +

EGFR, IC50: 1.2 μM

99%+
AG-556 +

EGFR, IC50: 5 μM

98%
RG13022 +

EGFR, IC50: 4 μM

99%+
Tyrphostin RG 14620 99%+
Vandetanib +

EGFR, IC50: 500 nM

99%
CNX-2006 ++

mutant EGFR, IC50: <20 nM

++

mutant EGFR, IC50: <20 nM

99%
AZD3759 ++++

EGFR (L858R), IC50: 0.2 nM

EGFR (WT), IC50: 0.3 nM

98%
Erlotinib ++++

EGFR, IC50: 2 nM

95%
Saracatinib +++

EGFR (L861Q), IC50: 4 nM

EGFR, IC50: 5 nM

99%+
AG1557 99%
Rociletinib ++

EGFR (L858R/T790M), Ki: 21.5 nM

EGFR (wt), Ki: 303.3 nM

98%
AG490 +

EGFR, IC50: 0.1 μM

98%
Cetuximab ++++

EGFR, Kd: 0.39 nM

95%
Osimertinib ++

WT EGFR, IC50: 12.92 nM

L858R/T790M EGFR, IC50: 11.44 nM

98%
Osimertinib mesylate 98% (Content MsOH 15.2-18.2%)
Chrysophanol mTOR 98%
PD153035 ++++

EGFR, Ki: 5.2 pM

99%+
Olmutinib BTK 99%+
WZ4002 ++++

EGFR (L858R/T790M), IC50: 8 nM

EGFR (L858R), IC50: 2 nM

99%+
Icotinib +++

EGFR, IC50: 5 nM

99%
Desmethyl Erlotinib HCl ++++

EGFR, IC50: 2 nM

98%
Cyasterone 99%+
PP 3 +

EGFR tyrosine kinase, IC50: 2.7 μM

98%
WZ8040 99%+
(-)-Epigallocatechin Gallate 99%
AG 18 +

EGFR, IC50: 35 μM

99%+
O-Desmethyl gefitinib ++

EGFR, IC50: 36 nM

99%
Falnidamol 99%+
AZ-5104 ++++

EGFR (L858R), IC50: 6 nM

EGFR (L861Q) , IC50: <1 nM

+++

ErbB4, IC50: 7 nM

BRK 99%+
Butein 95%
Genistein 98%
SU5214 +

EGFR, IC50: 36.7 μM

99%+
Naquotinib 99%+
Gefitinib ++

EGFR, IC50: 15.5 nM

+

EGFR (858R/T790M), IC50: 823.3 nM

98%
Theliatinib +++

WT EGFR, IC50: 3 nM

++

EGFR T790M/L858R, IC50: 22 nM

99%
Lazertinib ++++

WT EGFR, IC50: 76 nM

L858R/T790M EGFR, IC50: 2 nM

++++

Del19/T790M, IC50: 1.7 nM

99%+
Gefitinib-based PROTAC 3 ++

EGFR, DC50: 22.3 nM

99%+
MTX-211 PI3K 98%
(E)-AG 99 99%+
Licochalcone D PARP,Caspase 99%
Zipalertinib +++

EGFR WT, IC50: 8 nM

EGFR (L861Q), IC50: 4.1 nM

+++

HER4, IC50: 4 nM

++++

EGFR(d746-750), IC50: 1.4 nM

EGFR L858R, IC50: 2 nM

97%
JND3229 +++

EGFR WT, IC50: 6.8 nM

++

EGFR L858R/T790M, IC50: 30.5 nM

99%+
Firmonertinib mesylate 99%+
Tyrphostin AG30 99%+
EGFR-IN-12 ++

EGFR, IC50: 21 nM

99%+
Mobocertinib 98%
(Rac)-JBJ-04-125-02 95%
(S)-Sunvozertinib 99%
BLU-945 95%
Poziotinib +++

HER1, IC50: 3.2 nM

++

HER4, IC50: 23.5 nM

+++

HER2, IC50: 5.3 nM

98%
TAK-285 ++

EGFR/HER1, IC50: 23 nM

+

HER4, IC50: 260 nM

++

HER2, IC50: 17 nM

99%+
ARRY-380 analog 99%
Canertinib ++++

EGFR, IC50: 1.5 nM

+++

ErbB2, IC50: 9.0 nM

99%+
Dacomitinib +++

EGFR, IC50: 6.0 nM

+

ErbB4, IC50: 73.7 nM

+

ErbB2, IC50: 45.7 nM

98%
EGFR/ErbB-2/ErbB-4 inhibitor-2 +

ErbB4, IC50: 1.91 μM

+

ErbB2, IC50: 0.08 μM

99%+
(E/Z)-CP-724714 ++

HER2/ErbB2, IC50: 10 nM

95%
Lapatinib ++

EGFR, IC50: 10.8 nM

+

ErbB4, IC50: 367 nM

+++

ErbB2, IC50: 9.2 nM

98%
AEE788 ++++

EGFR, IC50: 2 nM

+

HER4/ErbB4, IC50: 160 nM

+++

HER2/ErbB2, IC50: 6 nM

c-Fms/CSF1R 98+%
AV-412 free base ++++

EGFR, IC50: 0.75 nM

++

ErbB2, IC50: 19 nM

++++

EGFRL858R/T790M, IC50: 0.51 nM

EGFRT790M, IC50: 0.79 nM

98+%
Neratinib +

EGFR, IC50: 92 nM

+

HER2, IC50: 59 nM

Src 98%
BMS-599626 ++

HER1, IC50: 20 nM

+

HER4, IC50: 190 nM

++

HER2, IC50: 30 nM

98%
Tucatinib +++

ErbB2, IC50: 8 nM

98%
Allitinib ++++

EGFR, IC50: 0.5 nM

++++

ErbB4, IC50: 0.8 nM

+++

ErbB2, IC50: 3.0 nM

99%
Pelitinib +

EGFR, IC50: 38.5 nM

+

ErbB2, IC50: 1.255 μM

Src,Raf 99%+
Sapitinib +++

EGFR, IC50: 4 nM

+++

ErbB3, IC50: 4 nM

+++

ErbB2, IC50: 3 nM

99%+
CUDC-101 +++

EGFR, IC50: 2.4 nM

++

HER2, IC50: 15.7 nM

HDAC 99%+
Varlitinib +++

ErbB1, IC50: 7 nM

++++

ErbB2, IC50: 2 nM

99%+
Afatinib dimaleate ++++

EGFR (L858R/T790M), IC50: 0.4 nM

EGFR (wt), IC50: 0.5 nM

++

HER2, IC50: 14 nM

98%
Canertinib 2HCl +++

EGFR, IC50: 7.4 nM

+++

ErbB2, IC50: 9 nM

99%
Allitinib tosylate ++++

EGFR (T790M/L858R), IC50: 12 nM

EGFR, IC50: 0.5 nM

++++

ErbB4, IC50: 0.8 nM

+++

ErbB2, IC50: 3.0 nM

99%
Tyrphostin AG 528 +

EGFR, IC50: 4.9 μM

+

HER2, IC50: 2.1 μM

97%
Afatinib ++++

EGFR (wt), IC50: 0.5 nM

EGFR (L858R), IC50: 10 nM

++++

ErbB4, IC50: 1 nM

++

HER2, IC50: 14 nM

99%
Pyrotinib dimaleate ++

EGFR, IC50: 0.013 μM

++

HER2, IC50: 0.038 μM

98%
Epertinib HCl ++++

EGFR, IC50: 1.48 nM

+++

HER4, IC50: 2.49 nM

+++

HER2, IC50: 7.15 nM

99%
Tuxobertinib ++++

EGFR, Kd: 0.2 nM

++++

HER2, Kd: 0.76 nM

99%
ALK-IN-1 ++

EGFR(del19), IC50: 36.8 nM

EGFR(C797S/del19), IC50: 138.6 nM

ALK 99%
Brigatinib +

EGFR(C797S/T790M/del19), IC50: 67.2 nM

EGFR(del19), IC50: 39.9 nM

ALK,FLT3 98%
Avitinib ++++

EGFR L858R/T790M, IC50: 0.18 nM

BTK 99%+
EAI045 97%
Almonertinib 99%
BI-4020 ++++

EGFRdel19 T790M C797S, IC50: 0.2 nM

99%+
EGFR-IN-7 ++++

EGFRL858R/T790M, IC50: 0.19 nM

EGFRd746-750/T790M/C797S, IC50: 0.26 nM

99%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。

Cetuximab/西妥昔单抗 生物活性

靶点
  • EGFR/ErbB1

    EGFR, Kd:0.39 nM

蛋白种属 Human
交叉反应性 Human,Mouse,Cynomolgus
Isotype IgG1-Kappa
内毒素 < 0.001EU/μg, determined by LAL method.
纯化方法 Purified, Protein A, affinity column
稀释缓冲液 Sterile PBS or 0.9% saline for reconstitution/dilution. It is recommended to use the reconstituted/diluted product within one month.

Cetuximab/西妥昔单抗 细胞实验

Cell Line
Concentration Treated Time Description References
NK cells 10 μg/mL 24 hours To evaluate the killing effect of NK cells on HNSCC cells in the presence of Lirilumab, results showed that Lirilumab significantly enhanced NK cell-mediated killing of tumor cells. Head Neck. 2019 Aug;41(8):2591-2601
IL-1R1 stable knockdown SQ20B cells 1, 10, and 100 μg/mL 48 h IL-1R1 knockdown significantly suppressed cetuximab-induced cytokine secretion. J Immunother Cancer. 2019 Mar 19;7(1):79
MyD88 stable knockdown SQ20B cells 1, 10, and 100 μg/mL 48 h MyD88 knockdown significantly suppressed cetuximab-induced cytokine secretion. J Immunother Cancer. 2019 Mar 19;7(1):79
SQ20B cells 1, 10, and 100 μg/mL 48 h Cetuximab at a dose of 100 μg/mL significantly increased IL-1α and IL-8 secretion, and increased IL-6 secretion at all tested concentrations. J Immunother Cancer. 2019 Mar 19;7(1):79
Cal-27 cells 1, 10, and 100 μg/mL 48 h Cetuximab at a dose of 100 μg/mL significantly increased IL-1α, IL-6, and IL-8 secretion. J Immunother Cancer. 2019 Mar 19;7(1):79
DLD-1 100 μg/ml 24 h To evaluate the cytotoxic and antiproliferative effects of Cetuximab combined with RSL3 on KRAS mutant CRC cells. Results showed that the combination treatment significantly inhibited cell viability and proliferation. Cell Death Dis. 2021 Nov 13;12(11):1079
HCT116 100 μg/ml 24 h To evaluate the cytotoxic and antiproliferative effects of Cetuximab combined with RSL3 on KRAS mutant CRC cells. Results showed that the combination treatment significantly inhibited cell viability and proliferation. Cell Death Dis. 2021 Nov 13;12(11):1079
C10 1 ng/µL 72 h To assess the efficacy of targeting the AURKA/YAP1 axis to overcome cetuximab resistance Br J Cancer. 2024 May;130(8):1402-1413
SW48 10 ng/µL 72 h To assess the efficacy of targeting the AURKA/YAP1 axis to overcome cetuximab resistance Br J Cancer. 2024 May;130(8):1402-1413
HCT116 cells 0.1 μM or 1 μM 24 h To evaluate the effect of Cetuximab on EGFR protein expression. Results showed that Cetuximab only marginally affected EGFR levels in HCT116 cells. J Nucl Med. 2018 Oct;59(10):1558-1565
H1975 cells 0.1 μM or 1 μM 24 h To evaluate the effect of Cetuximab on EGFR protein expression. Results showed that 0.1 μM Cetuximab reduced EGFR protein expression by 3-fold in H1975 cells, while the effect was slightly attenuated at the higher dose (1 μM). J Nucl Med. 2018 Oct;59(10):1558-1565
UMSCC 103 20 μM 48 h Test the cytotoxic effect of Cetuximab on UMSCC 103, finding significant cell death when combined with ICI Cell Death Dis. 2023 Sep 19;14(9):613
Patient-derived colorectal cancer organoids (PDXO) 20 μg/mL 72 h To evaluate the effect of cetuximab on BIM protein expression, results showed that cetuximab upregulated BIM protein levels. Clin Cancer Res. 2023 Mar 14;29(6):1102-1113
Patient-derived colorectal cancer organoids (PDXO) 20 μg/mL 1 week To evaluate the effect of cetuximab on PDXO cell viability, results showed that cetuximab inhibited cell growth. Clin Cancer Res. 2023 Mar 14;29(6):1102-1113

Cetuximab/西妥昔单抗 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Athymic nu/nu mice Cal-27 and SQ20B xenograft models Intraperitoneal injection 2 mg/kg Twice weekly for 2 weeks IL-1 blockade (using anakinra) did not affect the anti-tumor efficacy of cetuximab. J Immunother Cancer. 2019 Mar 19;7(1):79
BALB/c nude mice DLD-1 xenograft model Intraperitoneal injection 13 mg/kg Once daily for 17 days To evaluate the antitumor effects of Cetuximab combined with RSL3 on KRAS mutant CRC xenograft models. Results showed that the combination treatment significantly reduced tumor volume and increased MDA levels. Cell Death Dis. 2021 Nov 13;12(11):1079
Mice Patient-derived xenograft (PDX) models of KRAS-mutated colorectal cancer Intraperitoneal injection 25 mg/kg Twice weekly, for 28 days or longer To evaluate the efficacy of combined Cetuximab and Trametinib therapy in KRAS-mutated CRC PDX models. The combination therapy induced disease control (partial response or stable disease) in 74% of the models analyzed, with 47% achieving partial response. Mol Oncol. 2023 Nov;17(11):2396-2414
Nude mice Orthotopic HNSCC mouse model Intraperitoneal injection 40 mg/kg Every 3 days for 4 weeks Evaluate the effect of Cetuximab alone or in combination with ICI on HNSCC tumor growth, finding significant tumor growth delay with combination therapy Cell Death Dis. 2023 Sep 19;14(9):613
BALB/c nude mice H1975 tumor model (non-small cell lung cancer) and HCT116 tumor model (colorectal cancer) Intravenous injection (Cetuximab) or intraperitoneal injection (Gemcitabine) 10 mg/kg Cetuximab was administered on day 1 or days 1 and 2, Gemcitabine on day 2, and imaging was performed on day 3. To evaluate the effect of Cetuximab alone or in combination with Gemcitabine on tumor growth and biological markers. Results showed that repeated doses of Cetuximab significantly increased 18F-ICMT-11 uptake and cleaved caspase-3 staining in H1975 tumors, while a single dose was insufficient to induce apoptosis but affected proliferation. 18F-FLT uptake was significantly reduced, paralleled by a decrease in Ki-67 and marked tumor growth delay. HCT116 tumors were insensitive to Cetuximab treatment. J Nucl Med. 2018 Oct;59(10):1558-1565
NSG mice CDX-humanized mouse model Intravenous injection 0.4 mg/kg/dose Weekly for 5 weeks Evaluate the antitumor effects of cetuximab in combination with NK cells J Immunother Cancer. 2024 Mar 27;12(3):e008585
NOD/SCID mice Patient-derived xenograft models (PDX) Intraperitoneal injection 20 mg/kg Twice weekly for 5 weeks To evaluate the effect of cetuximab on tumor volume in PDX models, results showed that cetuximab significantly reduced tumor volume. Clin Cancer Res. 2023 Mar 14;29(6):1102-1113

Cetuximab/西妥昔单抗 技术信息

CAS号205923-56-4
分子量 145.56 kDa
SMILES Code NONE
MDL No. MFCD06407972
别名 C225
运输蓝冰
存储条件

In solvent -20°C:3-6个月-80°C:24个月

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