Ambeed.cn

首页 / / / / Lapatinib/拉帕替尼

Lapatinib/拉帕替尼 {[allProObj[0].p_purity_real_show]}

货号:A254504 同义名: GW572016; GW2016

Lapatinib(GW572016)对ErbB-2和EGFR酪氨酸激酶结构域具有强效抑制作用,对纯化EGFR和ErbB-2的IC50值分别为10.2 nM和9.8 nM。

Lapatinib/拉帕替尼 化学结构 CAS号:231277-92-2
Lapatinib/拉帕替尼 化学结构
CAS号:231277-92-2
Lapatinib/拉帕替尼 3D分子结构
CAS号:231277-92-2
Lapatinib/拉帕替尼 化学结构 CAS号:231277-92-2
Lapatinib/拉帕替尼 3D分子结构 CAS号:231277-92-2
规格 价格 会员价 库存 数量
{[ item.pr_size ]}

{[ getRatePriceInt(item.pr_rmb, 1,1) ]}

{[ getRatePriceInt(item.pr_rmb_sale, 1,1) ]} {[ suihuo_tips(item.pr_tag_price, item.pr_am) ]}

{[ getRatePriceInt(item.pr_rmb, 1,1) ]}

{[ getRatePriceInt(item.pr_rmb,item.pr_rate,1) ]} {[ suihuo_tips(item.pr_tag_price, item.pr_am) ]}
{[ getRatePriceInt(item.pr_rmb, 1,1) ]}{[ suihuo_tips(item.pr_tag_price, item.pr_am) ]} {[ getRatePrice(item.pr_rmb_sale, 1,1,item.mem_isinteger) ]} {[ getRatePrice(item.pr_rmb,item.pr_rate,item.mem_rate,item.mem_isinteger) ]} {[ getRatePrice(item.pr_rmb,1,item.mem_rate,item.mem_isinteger) ]} 现货 1周 咨询 - +
购物车0 收藏 询单

Lapatinib/拉帕替尼 纯度/质量文件 产品仅供科研

货号:A254504 标准纯度: {[allProObj[0].p_purity_real_show]}
批次查询: 批次纯度:

全球学术期刊中引用的产品

Nature, 2025, 645, 793-800. Ambeed. [ A201204 , A444152 , A344107 , A952055 ]
Cell, 2025. Ambeed. [ A122167 ]
Science, 2025, 387(6729): eadp5637. Ambeed. [ A875019 ]
Sig. Transduct. Target. Ther., 2025, 10, 257. Ambeed. [ A104916 ]
Nat. Nanotechnol., 2025. Ambeed. [ A243018 , A1216705 , A522597 , A125401 , A1355641 ]
更多 >
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

PKC,PKA 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

VEGFR,Src 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 ++

L858R/T790M EGFR, IC50: 11.44 nM

WT EGFR, IC50: 12.92 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), IC50: 2 nM

EGFR (L858R/T790M), IC50: 8 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 ++++

L858R/T790M EGFR, IC50: 2 nM

WT EGFR, IC50: 76 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 (L861Q), IC50: 4.1 nM

EGFR WT, IC50: 8 nM

+++

HER4, IC50: 4 nM

++++

EGFR L858R, IC50: 2 nM

EGFR(d746-750), IC50: 1.4 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 (wt), IC50: 0.5 nM

EGFR (L858R/T790M), IC50: 0.4 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(del19), IC50: 39.9 nM

EGFR(C797S/T790M/del19), IC50: 67.2 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。
产品名称 HER2 其他靶点 纯度
Poziotinib ++++

HER2, IC50: 5.3 nM

98%
Tyrphostin AG 879 +

HER2-Neu, IC50: 1.0 μM

95%
TAK-285 +

HER2, IC50: 17 nM

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

ErbB2, IC50: 9.0 nM

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

HER2/ErbB2, IC50: 10 nM

95%
Lapatinib +++

ErbB2, IC50: 9.2 nM

EGFR 98%
AEE788 ++++

HER2/ErbB2, IC50: 6 nM

EGFR 98+%
Neratinib +

HER2, IC50: 59 nM

EGFR,Src 98%
BMS-599626 +

HER2, IC50: 30 nM

98%
Mubritinib ++++

HER2/ErbB2, IC50: 6.0 nM

99%+
Tucatinib +++

ErbB2, IC50: 8 nM

98%
Sapitinib ++++

ErbB2, IC50: 3 nM

EGFR 99%+
CUDC-101 ++

HER2, IC50: 15.7 nM

EGFR,HDAC 99%+
Afatinib dimaleate ++

HER2, IC50: 14 nM

98%
Afatinib ++

HER2, IC50: 14 nM

99%
Pertuzumab 95%
Trastuzumab 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。

Lapatinib/拉帕替尼 生物活性

靶点
  • EGFR/ErbB1

    EGFR, IC50:10.8 nM

  • HER2/ErbB2

    ErbB2, IC50:9.2 nM

  • ErbB4

    ErbB4, IC50:367 nM

  • HER2

    ErbB2, IC50:9.2 nM

描述 EGFR (epidermal growth factor receptor) family consists of four members that belong to the ErbB lineage of proteins (ErbB1 - 4) with an external domain that binds activating ligands, such as EGF, and is overexpressed in a significant percentage of carcinomas and contributes to the malignant phenotype. Upon activation, EGFR phosphorylates both the receptor itself and a variety of “effector” protein. Lapatinib is a dual inhibitor of both EGFR and ErbB2 with IC50 values of 10.8 nM and 9.2 nM (measured by kinase activity), respectively, 300-fold selective over other kinases tested except for ErbB-4 (IC50 = 367 nM). Treatment with Lapatinib for 6h inhibited receptor autophosphorylation of EGFR and ErbB-2, as well as phosphorylation of serine-473 of AKT, the key signal transduction mediator, in a dose-responsive manner at concentration ranged from 0.03 to 10 μM in BT474 and HN5 cell lines. Lapatinib showed growth inhibition with IC50 values ranged from 0.09 - 12μM in EGFR-overexpressing cell lines HN5 and A-431, the ErbB-2-overexpressing cell lines BT474, N87 and CaLu-3,as well as tumor cell lines expressing low levels of EGFR and ErbB-2, MCF-7 and T47D cells. Treatment with 1 and 10 μM Lapatinib resulted in induction of G1 arrest and increased number of cells with sub-2N DNA content, consistent with cell death by an apoptotic mechanism, in EGFR-overexpressing cell line, HN5, and BT474 cells. Complete inhibition of tumor growth was seen at dose of 100mg/kg, orally, twice daily, in BT474 and HN5 human tumor xenografts[1].
作用机制 Lapatinib binds reversibly and a very slow off-rate to the ATP binding pocket in an inactive-like conformation, thus preventing autophosphorylation of the target[2].

Lapatinib/拉帕替尼 细胞实验

Cell Line
Concentration Treated Time Description References
SKBR3 10 nM 72 h To evaluate the effect of Lapatinib in combination with Trastuzumab on HER2-positive breast cancer cells, results showed cell cycle arrest at G1 and reduced clonogenic potential. Nat Commun. 2020 Jan 20;11(1):385.
BT474 10 nM 72 h To evaluate the effect of Lapatinib in combination with Trastuzumab on HER2-positive breast cancer cells, results showed cell cycle arrest at G1 and reduced clonogenic potential. Nat Commun. 2020 Jan 20;11(1):385.
SKBR3 10 nM 72 h To evaluate the effects of dual HER2 blockade on SKBR3 cells, results showed a significant relative increase in Luminal A and normal-like signature scores, and a relative decrease in proliferation, HER2-E, Luminal B and Basal-like signature scores. Nat Commun. 2020 Jan 20;11(1):385.
BT474 10 nM 72 h To evaluate the effects of dual HER2 blockade on BT474 cells, results showed a significant relative increase in Luminal A and normal-like signature scores, and a relative decrease in proliferation, HER2-E, Luminal B and Basal-like signature scores. Nat Commun. 2020 Jan 20;11(1):385.
BT474 cells 1 μM 1 hour Lapatinib inhibited the phosphorylation of FASN in BT474 cells and suppressed HRG-induced FASN activity. Breast Cancer Res. 2010;12(6):R96.
SKBR3 cells 1 μM 1 hour Lapatinib inhibited the phosphorylation of FASN in SKBR3 cells and suppressed HRG-induced FASN activity. Breast Cancer Res. 2010;12(6):R96.
HT-29 colorectal cancer cells 6 μM 24 h To study the inhibitory effect of Sorafenib on the phosphorylation of CSE1L and ERK1/2. The results showed that Sorafenib treatment inhibited ERK1/2 phosphorylation and reduced the levels of hyper- and hypo-phosphorylated CSE1L. J Transl Med. 2015 Jun 13;13:191.

Lapatinib/拉帕替尼 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
BALB/c-null mice MCF7 tumor model Intravenous injection 2 mg/kg Day 0, 2, 4, 6, for 18 days To evaluate the in vivo anticancer efficacy of LJ@Trp-NPs, the results showed that LJ@Trp-NPs significantly inhibited tumor growth and enhanced the anticancer effect of Lapatinib. Bioact Mater. 2021 Jul 14;9:15-28.
BALB/c-null mice MCF7 tumor model Intravenous injection 2 mg/kg Administered on days 0, 2, 4, and 6, lasting for 18 days To evaluate the synergistic anticancer effect of Lapatinib and JPH203 on MCF7 tumor-bearing mice, results showed significant tumor growth inhibition. Bioact Mater. 2021 Jul 14;9:15-28.
Nude mice SGC031 PDGCX model Oral 100 mg/kg Twice daily for 3 weeks In the SGC031 PDGCX model, Lapatinib did not show significant tumor growth inhibition, with a TGI of 17%. Br J Cancer. 2014 Mar 4;110(5):1169-78.
NOD SCID mice HT-29 colorectal tumor xenograft model Oral 60 mg/kg Once daily for 10 days To study the anti-tumor effect of Lapatinib in the HT-29 colorectal tumor xenograft model. The results showed that Lapatinib treatment significantly inhibited tumor growth and reduced serum phospho-CSE1L levels 3 days after treatment. J Transl Med. 2015 Jun 13;13:191.
NOD/SCID mice MCF-10CA1a-HER2 overexpressing cell model Oral 100 mg/kg Lapatinib, 25 mg/kg BYL719 Once daily for 3 weeks To evaluate the inhibitory effects of Lapatinib and BYL719 alone or in combination on PIK3CAH1047R mutant tumors. The results showed that combination therapy significantly inhibited tumor growth. Clin Transl Med. 2021 Nov;11(11):e589
Balb/c nude mice CWR22 and 22Rv1 human tumor xenograft models Oral gavage 50 mg/kg 5 days per week until tumor volume exceeded 150 mm³ or study endpoint To assess the antitumor efficacy of lapatinib in androgen-sensitive and castration-resistant prostate cancer models. Results demonstrated that lapatinib failed to significantly inhibit tumor growth in CWR22 or 22Rv1 models but increased intratumoral HER2 protein levels. Br J Cancer. 2019 Jul;121(3):237-248

Lapatinib/拉帕替尼 动物研究

Dose Rat (p.o.): 50 mg/kg - 500 mg/kg[3]
Administration p.o.
Pharmacokinetics
Animal Mice[4] Rats[4] Dogs[4]
Dose 10 mg/kg 10 mg/kg 10 mg/kg
Administration i.v. i.v. i.v.
Cmax 942 ng/ml 4557 ± 1210 ng/ml 3793 ± 167 ng/ml
T1/2 5.69 h 12.3 ± 8.24 h 5.85 ± 0.17 h
CL 48.0 ml/min/kg 48.8 ± 14.3 ml/min/kg 12.2 ± 2.83 ml/min/kg
Tmax 0.5 h 0.08 h 0.08 h
Vss 9.55 L/kg 6.16 ± 1.95 L/kg 5.70 ± 1.03 L/kg
AUC 3469 ng·h/ml 3596 ± 924 ng·h/ml 14087 ± 3094 ng·h/ml

Lapatinib/拉帕替尼 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT00555152 Ductal Breast Carcinoma In Sit... 展开 >>u HER2/Neu Positive 收起 << Not Applicable Completed - United States, Alabama ... 展开 >> University of Alabama at Birmingham Cancer Center Birmingham, Alabama, United States, 35233 United States, Texas M D Anderson Cancer Center Houston, Texas, United States, 77030 收起 <<
NCT00555152 - Completed - -
NCT00999804 Breast Cancer Phase 2 Active, not recruiting January 2018 United States, Alabama ... 展开 >> University of Alabama - Birmingham Birmingham, Alabama, United States, 35294 United States, Illinois University of Chicago Chicago, Illinois, United States, 60637 United States, Indiana Indiana University Indianapolis, Indiana, United States, 46202 United States, Maryland Johns Hopkins Baltimore, Maryland, United States, 21231 United States, Massachusetts Dana Farber Cancer Institute Boston, Massachusetts, United States, 02130 United States, North Carolina Duke University Durham, North Carolina, United States, 27705 United States, Tennessee Vanderbilt University Medical Center Nashville, Tennessee, United States, 37212 United States, Texas Baylor College of Medicine Lester and Sue Smith Breast Center Houston, Texas, United States, 77030 收起 <<

Lapatinib/拉帕替尼 参考文献

[1]Rusnak DW, Lackey K, et al. The effects of the novel, reversible epidermal growth factor receptor/ErbB-2 tyrosine kinase inhibitor, GW2016, on the growth of human normal and tumor-derived cell lines in vitro and in vivo. Mol Cancer Ther. 2001 Dec;1(2):85-94.

[2]Wood ER, Truesdale AT, et al. A unique structure for epidermal growth factor receptor bound to GW572016 (Lapatinib): relationships among protein conformation, inhibitor off-rate, and receptor activity in tumor cells. Cancer Res. 2004 Sep 15;64(18):6652-9.

[3]ASSESSMENT REPORT FOR TYVERB

[4]Pharmacokinetics of lapatinib

Lapatinib/拉帕替尼 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

1.72mL

0.34mL

0.17mL

8.60mL

1.72mL

0.86mL

17.21mL

3.44mL

1.72mL

Lapatinib/拉帕替尼 技术信息

CAS号231277-92-2
分子式C29H26ClFN4O4S
分子量 581.06
SMILES Code CS(CCNCC(O1)=CC=C1C2=CC(C(NC3=CC(Cl)=C(OCC4=CC(F)=CC=C4)C=C3)=NC=N5)=C5C=C2)(=O)=O
MDL No. MFCD09264194
别名 GW572016; GW2016; GSK572016
运输蓝冰
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, inert atmosphere, room temperature

溶解方案

DMSO: 120 mg/mL(206.52 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂:
——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
方案 一
方案 二
AmBeed 相关网站 AmBeed.cn AmBeed.com
AmBeed
关于我们
联系我们
资讯中心
网站地图
产品手册
  • 批次文件查询
  • 客户支持
    技术支持
    专业术语
    缩略词释义
    质量手册
    产品咨询
    计算器
    活动政策
    订购方法
    积分商城
    活动声明
    联系我们
    400-920-2911 sales@ambeed.cn tech@ambeed.cn
    AmBeed 只为有资质的科研机构、医药企业基于科学研究或药证申报的用途提供医药研发服务,不为任何个人或者非科研性质用途提供服务。