AZD3759 | EGFR | AmBeed-信号通路专用抑制剂

AZD3759 {[allProObj[0].p_purity_real_show]}

货号：A171107

AZD3759是一种EGFR抑制剂，能抑制EGFR（野生型）、EGFR（L858R突变）以及EGFR（外显子19缺失），IC50分别为0.3 nM、0.2 nM和0.2 nM。

AZD3759 化学结构
CAS号：1626387-80-1

AZD3759 3D分子结构
CAS号：1626387-80-1

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EGFR 亚型比较

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	++++ EGFR^L858R/T790M, IC50: 0.51 nM EGFR^T790M, 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					++++ EGFR^{del19 T790M C797S}, IC50: 0.2 nM		99%+
EGFR-IN-7					++++ EGFR^L858R/T790M, IC50: 0.19 nM EGFR^{d746-750/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。

AZD3759 生物活性

靶点

EGFR/ErbB1

EGFR (L858R), IC50:0.2 nM

EGFR (WT), IC50:0.3 nM

描述

Zorifertinib (AZD3759) is a highly potent, orally bioavailable EGFR inhibitor with the ability to penetrate the central nervous system. It demonstrates remarkable efficacy against EGFR mutations, exhibiting IC50 values of 0.3 nM for wild-type EGFR (EGFRwt), 0.2 nM for EGFR with the L858R mutation (EGFRL858R), and 0.2 nM for EGFR with an exon 19 deletion (EGFRexon 19Del) at ATP concentrations equivalent to Km. Zorifertinib effectively induces apoptosis in cancer cells and shows significant antitumor activity, making it a valuable candidate for research into non-small cell lung cancer (NSCLC), hepatocellular carcinoma (HCC), and potentially other malignancies^[1].

体内研究

Pharmacokinetic studies reveal that Zorifertinib is rapidly absorbed following oral administration in rats, achieving a maximum blood concentration (Cmax) of 0.58 μM within an hour. The drug then exhibits a monoexponential decline in blood concentrations with an elimination half-life of approximately 4.3 hours, closely mirroring the half-life observed with intravenous administration (4.1 hours). Notably, the bioavailability of Zorifertinib after oral dosing in rats is reported at 91%. Similar pharmacokinetic profiles are observed in male dogs, with rapid absorption and a Cmax reached between 0.5 to 1.5 hours post-oral administration, a clearance rate of 14 mL/min per kg, a volume of distribution of 6.4 L/kg, and an elimination half-life of 6.2 hours. The oral bioavailability in dogs is excellent at 90%^[1].

Zorifertinib has demonstrated significant antitumor efficacy in preclinical models, achieving 78% tumor growth inhibition at a daily dose of 7.5 mg/kg and tumor regression at 15 mg/kg daily, 4 weeks post-treatment, without causing more than 20% body weight loss. This contrasts with limited effects observed from CP-358774 in the same model. Decreases in tumor area were notably seen with Zorifertinib doses of 7.5 and 15 mg/kg. Additionally, modulation of pEGFR was confirmed through a single dose of Zorifertinib (15 mg/kg), taken 1 hour post-dosing, further evidencing the drug's target engagement^[1].

体外研究

At higher ATP concentrations (2 mM), the IC50 values adjust to 102 nM for EGFRwt, 7.6 nM for EGFRL858R, and 2.4 nM for EGFRexon 19Del, respectively. Furthermore, Zorifertinib inhibits phosphorylated EGFR (pEGFR) in various cell lines, including H838wt, H3255L858R, and PC-9exon 19Del, with IC50s of 64.5, 7.2, and 7.4 nM, respectively. In cellular phosphorylation assays, Zorifertinib also displays a 9-fold selectivity in inhibiting EGFR-mutant cell lines over wild-type EGFR cell lines (using the H838 cell line as a reference)^[1].

AZD3759 细胞实验

Cell Line Rat liver hepatocytes (RLHs) Rat liver microsomes (RLMs) A549 nonsmall lung carcinoma cells C6-LUC cells U87 cells C6 cells Primary mouse cortical neurons H3255 cells PC-9 cells	Concentration	Treated Time	Description	References
Rat liver hepatocytes (RLHs)	30 μM	2 hours	Detection of in vitro metabolites of ZFB	RSC Adv. 2022 Jul 21;12(32):20991-21003.
Rat liver microsomes (RLMs)	30 μM	90 minutes	Detection of in vitro metabolites and reactive intermediates of ZFB	RSC Adv. 2022 Jul 21;12(32):20991-21003.
A549 nonsmall lung carcinoma cells	28.67 ± 5.69		Evaluate the antiproliferative effects of AZD3759 and its derivative 7 on A549 cells, showing an IC50 value of 6.10 ±0.13 μM for 7.	ACS Med Chem Lett. 2018 Dec 6;10(1):22-26.
C6-LUC cells	1, 2, 4 μM	24 hours	To evaluate the effect of AZD3759 on the cell cycle of C6-LUC cells, the results showed that AZD3759 significantly increased the proportion of cells in the G0/G1 phase.	Bioengineered. 2021 Dec;12(1):8679-8689.
U87 cells	1, 2, 4 μM	10-14 days	To evaluate the inhibitory effect of AZD3759 on the proliferation of U87 cells, the results showed that AZD3759 significantly reduced the survival fraction of U87 cells in a dose-dependent manner.	Bioengineered. 2021 Dec;12(1):8679-8689.
C6 cells	1, 2, 4 μM	10-14 days	To evaluate the inhibitory effect of AZD3759 on the proliferation of C6 cells, the results showed that AZD3759 significantly reduced the survival fraction of C6 cells in a dose-dependent manner.	Bioengineered. 2021 Dec;12(1):8679-8689.
Primary mouse cortical neurons	0.63 nM and 8.4 nM	4 hours	To evaluate the effect of AZD3759 on α-syn-PFFs uptake, results showed AZD3759 reduced α-syn-PFFs uptake	Neurotherapeutics. 2021 Apr;18(2):979-997.
H3255 cells	500 nM	30 minutes	Evaluate the effect of AZD3759 on the sensitivity of NSCLC cells to radiation, results showed AZD3759 significantly enhanced RA-induced apoptosis and DNA damage	Bioengineered. 2022 Jan;13(1):331-344.
PC-9 cells	500 nM	30 minutes	Evaluate the effect of AZD3759 on the sensitivity of NSCLC cells to radiation, results showed AZD3759 significantly enhanced RA-induced apoptosis and DNA damage	Bioengineered. 2022 Jan;13(1):331-344.

Cell Line

Rat liver hepatocytes (RLHs) Rat liver microsomes (RLMs) A549 nonsmall lung carcinoma cells C6-LUC cells U87 cells C6 cells Primary mouse cortical neurons H3255 cells PC-9 cells

Concentration

Treated Time

Description

References

Rat liver hepatocytes (RLHs)

30 μM

2 hours

Detection of in vitro metabolites of ZFB

RSC Adv. 2022 Jul 21;12(32):20991-21003.

Rat liver microsomes (RLMs)

30 μM

90 minutes

Detection of in vitro metabolites and reactive intermediates of ZFB

RSC Adv. 2022 Jul 21;12(32):20991-21003.

A549 nonsmall lung carcinoma cells

28.67 ± 5.69

Evaluate the antiproliferative effects of AZD3759 and its derivative 7 on A549 cells, showing an IC50 value of 6.10 ±0.13 μM for 7.

ACS Med Chem Lett. 2018 Dec 6;10(1):22-26.

C6-LUC cells

1, 2, 4 μM

24 hours

To evaluate the effect of AZD3759 on the cell cycle of C6-LUC cells, the results showed that AZD3759 significantly increased the proportion of cells in the G0/G1 phase.

Bioengineered. 2021 Dec;12(1):8679-8689.

U87 cells

1, 2, 4 μM

10-14 days

To evaluate the inhibitory effect of AZD3759 on the proliferation of U87 cells, the results showed that AZD3759 significantly reduced the survival fraction of U87 cells in a dose-dependent manner.

Bioengineered. 2021 Dec;12(1):8679-8689.

C6 cells

1, 2, 4 μM

10-14 days

To evaluate the inhibitory effect of AZD3759 on the proliferation of C6 cells, the results showed that AZD3759 significantly reduced the survival fraction of C6 cells in a dose-dependent manner.

Bioengineered. 2021 Dec;12(1):8679-8689.

Primary mouse cortical neurons

0.63 nM and 8.4 nM

4 hours

To evaluate the effect of AZD3759 on α-syn-PFFs uptake, results showed AZD3759 reduced α-syn-PFFs uptake

Neurotherapeutics. 2021 Apr;18(2):979-997.

H3255 cells

500 nM

30 minutes

Evaluate the effect of AZD3759 on the sensitivity of NSCLC cells to radiation, results showed AZD3759 significantly enhanced RA-induced apoptosis and DNA damage

Bioengineered. 2022 Jan;13(1):331-344.

PC-9 cells

500 nM

30 minutes

Evaluate the effect of AZD3759 on the sensitivity of NSCLC cells to radiation, results showed AZD3759 significantly enhanced RA-induced apoptosis and DNA damage

Bioengineered. 2022 Jan;13(1):331-344.

AZD3759 动物实验

Species Mice Sprague Dawley rats ICR mice C57BL6/C3H F1 mice Nude mice	Animal Model Traumatic brain injury (TBI) model Metabolic cages C6-LUC xenograft model Α-syn propagation mouse model PC-9-LUC brain metastasis model	Administration	Dosage	Frequency	Description	References
Mice	Traumatic brain injury (TBI) model	Oral	15 mg/kg	Daily administration for 14 days	AZD3759 promoted the recovery of body weight and neurological function in TBI mice, reduced astrocyte activation and EGFR expression, decreased chondroitin sulfate proteoglycans deposition, and upregulated GAP43 levels in the cortex.	Drug Des Devel Ther. 2024 Apr 16;18:1175-1188
Sprague Dawley rats	Metabolic cages	Oral gavage	10 mg/kg	Once daily for 120 hours	Detection of in vivo metabolites of ZFB	RSC Adv. 2022 Jul 21;12(32):20991-21003.
ICR mice	C6-LUC xenograft model	Oral	15, 30, 60 mg/kg	Once daily for 3 weeks	To evaluate the anti-tumor effect of AZD3759 on the C6-LUC xenograft model, the results showed that AZD3759 significantly inhibited tumor growth in a dose-dependent manner and was superior to osimertinib.	Bioengineered. 2021 Dec;12(1):8679-8689.
C57BL6/C3H F1 mice	Α-syn propagation mouse model	Oral gavage	15 mg/kg/day	Once daily for 21 days	To evaluate the effect of AZD3759 on α-syn pathology, results showed AZD3759 reduced pSyn pathology	Neurotherapeutics. 2021 Apr;18(2):979-997.
Nude mice	PC-9-LUC brain metastasis model	Oral	15 mg/kg/day	Once daily for 3 weeks	Evaluate the effect of AZD3759 on RA's inhibition of PC-9 cell brain metastasis, results showed AZD3759 significantly enhanced the antitumor effects of RA	Bioengineered. 2022 Jan;13(1):331-344.

Species

Mice Sprague Dawley rats ICR mice C57BL6/C3H F1 mice Nude mice

Animal Model

Traumatic brain injury (TBI) model Metabolic cages C6-LUC xenograft model Α-syn propagation mouse model PC-9-LUC brain metastasis model

Administration

Dosage

Frequency

Description

References

Mice

Traumatic brain injury (TBI) model

Oral

15 mg/kg

Daily administration for 14 days

AZD3759 promoted the recovery of body weight and neurological function in TBI mice, reduced astrocyte activation and EGFR expression, decreased chondroitin sulfate proteoglycans deposition, and upregulated GAP43 levels in the cortex.

Drug Des Devel Ther. 2024 Apr 16;18:1175-1188

Sprague Dawley rats

Metabolic cages

Oral gavage

10 mg/kg

Once daily for 120 hours

Detection of in vivo metabolites of ZFB

RSC Adv. 2022 Jul 21;12(32):20991-21003.

ICR mice

C6-LUC xenograft model

Oral

15, 30, 60 mg/kg

Once daily for 3 weeks

To evaluate the anti-tumor effect of AZD3759 on the C6-LUC xenograft model, the results showed that AZD3759 significantly inhibited tumor growth in a dose-dependent manner and was superior to osimertinib.

Bioengineered. 2021 Dec;12(1):8679-8689.

C57BL6/C3H F1 mice

Α-syn propagation mouse model

Oral gavage

15 mg/kg/day

Once daily for 21 days

To evaluate the effect of AZD3759 on α-syn pathology, results showed AZD3759 reduced pSyn pathology

Neurotherapeutics. 2021 Apr;18(2):979-997.

Nude mice

PC-9-LUC brain metastasis model

Oral

15 mg/kg/day

Once daily for 3 weeks

Evaluate the effect of AZD3759 on RA's inhibition of PC-9 cell brain metastasis, results showed AZD3759 significantly enhanced the antitumor effects of RA

Bioengineered. 2022 Jan;13(1):331-344.

AZD3759 参考文献

AZD3759 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.17mL

0.43mL

0.22mL

10.87mL

2.17mL

1.09mL

21.74mL

4.35mL

2.17mL

AZD3759 技术信息

CAS号	1626387-80-1
分子式	C₂₂H₂₃ClFN₅O₃
分子量	459.9
SMILES Code	O=C(N1[C@H](C)CN(C)CC1)OC2=CC3=C(NC4=CC=CC(Cl)=C4F)N=CN=C3C=C2OC
MDL No.	MFCD29058564

别名
运输	蓝冰
InChI Key	MXDSJQHFFDGFDK-CYBMUJFWSA-N
Pubchem ID	78209992

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, 2-8°C

溶解方案

细胞实验：

DMSO: 50 mg/mL(108.72 mM)，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

动物实验：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

方案三

方案四

细胞研究

细胞系	浓度	检测类型	检测时间	活性说明	数据源

H3255 cells	Proliferation assay	72 h	Antiproliferative against human H3255 cells expressing EGFR L858R mutant after 72 hrs by MTS assay, IC50=0.007 μM	26313252
H838 cells	Function assay		Inhibition of EGFR phosphorylation in human H838 cells, IC50=0.0645 μM	26313252
PC9 cells	Function assay		Inhibition of EGFR exon19 deletion mutant phosphorylation in human PC9 cells, IC50=0.0074 μM	26313252

AZD3759 {[allProObj[0].p_purity_real_show]}

AZD3759 纯度/质量文件产品仅供科研

全球学术期刊中引用的产品

AZD3759 质控信息

AZD3759 生物活性

AZD3759 细胞实验

AZD3759 动物实验

AZD3759 参考文献

AZD3759 实验方案

AZD3759 技术信息

最近浏览的产品

大规格询价

摩尔计算器

靶点

总药量计算器

工作液计算器

细胞研究

临床研究

确认信息

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AZD3759 {[allProObj[0].p_purity_real_show]}

AZD3759 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

AZD3759 质控信息

AZD3759 生物活性

AZD3759 细胞实验

AZD3759 动物实验

AZD3759 参考文献

AZD3759 实验方案

AZD3759 技术信息

最近浏览的产品

大规格询价

摩尔计算器

靶点

总药量计算器

工作液计算器

细胞研究

临床研究

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