Osimertinib mesylate | AZD-9291 mesylate;Mereletinib mesylate | AZD-9291 甲磺酸盐 | EGFR

Osimertinib mesylate/奥希替尼甲磺酸盐 {[allProObj[0].p_purity_real_show]}

货号：A188322 同义名： AZD-9291 甲磺酸盐 / AZD-9291 mesylate; Mereletinib mesylate

Osimertinib mesylate (AZD9291 mesylate) 是一种共价、口服活性、不可逆且选择性靶向突变的 EGFR 抑制剂，对 L858R 的表观 IC50 为 12 nM，对 L858R/T790M 的表观 IC50 为 1 nM。它能够克服 T790M 介导的对 EGFR 抑制剂的耐药性，用于治疗肺癌。

Osimertinib mesylate/奥希替尼甲磺酸盐化学结构
CAS号：1421373-66-1

Osimertinib mesylate/奥希替尼甲磺酸盐 3D分子结构
CAS号：1421373-66-1

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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。

Osimertinib mesylate/奥希替尼甲磺酸盐生物活性

靶点

EGFR/ErbB1

描述

Osimertinib mesylate (AZD9291 mesylate) is a covalent, orally active, irreversible EGFR inhibitor selective for mutant forms, with an IC50 of 12 nM against the L858R mutation and 1 nM against the L858R/T790M mutation. Otherwise, Osimertinib overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer^[1].

体内研究

In a preclinical model, osimertinib significantly reduces tumor volume in mice bearing C/L858R mutation tumors within days of treatment at 5 mg/kg/day, demonstrating nearly an 80% reduction in tumor volume as assessed by MRI, in stark contrast to vehicle-treated mice which showed tumor growth^[1].

Osimertinib has shown promising pharmacokinetics in rats, reduced affinity for hERG, and improved safety margins over previous compounds, leading to its selection for further development. Its dosing in efficacy models showed comparable results at relatively low doses (10 mg/kg per day), with excellent efficacy also noted at 5 mg/kg per day^[2].

体外研究

Osimertinib exhibits similar efficacy to early-generation tyrosine kinase inhibitors (TKIs) in inhibiting EGFR phosphorylation in cells harboring sensitive EGFR mutations, including PC-9 (ex19del), H3255 (L858R), and H1650 (ex19del), with mean IC50 values between 13 and 54 nM. It also effectively inhibits EGFR phosphorylation in T790M mutant cell lines (H1975 (L858R/T790M), PC-9VanR (ex19del/T790M)) with mean IC50 values below 15 nM^[1].

作用机制

Osimertinib may bind to T790M EGFR kinase in the ATP-binding domain (such as T790M and C797S).^[3]

Osimertinib mesylate/奥希替尼甲磺酸盐细胞实验

Cell Line PC9 H1975 HCC827 HCC827 H1975 cells EGFR-mutant lung adenocarcinoma cells PC9, H1975, HCC827, HCC2935 PC9, H1975, HCC827, HCC2935 PC9 cells H1975 cells	Concentration	Treated Time	Description	References
PC9	1uM	24 h	To evaluate the effect of Osimertinib on EGFR, AKT, and ERK signaling pathways, results showed that in resistant cells, EGFR signaling was suppressed, but ERK and AKT signaling was enhanced, and apoptosis was reduced.	Nat Med. 2019 Jan;25(1):111-118.
H1975	1uM	24 h	To evaluate the effect of Osimertinib on EGFR, AKT, and ERK signaling pathways, results showed that in resistant cells, EGFR signaling was suppressed, but ERK and AKT signaling was enhanced, and apoptosis was reduced.	Nat Med. 2019 Jan;25(1):111-118.
HCC827	0.01–2 µM	3 days	To observe the acute treatment response of HCC827 cells to Osimertinib, it was found that a subpopulation of tumor cells survived the initial treatment.	Nat Metab. 2019 Apr;1(4):460-474.
HCC827	160 nM	2–3 weeks	To observe the survival of HCC827 cells under continuous exposure to 160 nM Osimertinib, it was found that a small percentage of cells could survive for more than 2-3 weeks.	Nat Metab. 2019 Apr;1(4):460-474.
H1975 cells	0.1 μM	72 h	Osimertinib inhibited the growth of H1975 cells by 28 ± 13%	Biomark Res. 2021 Sep 6;9(1):69.
EGFR-mutant lung adenocarcinoma cells	0.1 μM	72 h	Osimertinib inhibited the growth of EGFR-mutant lung adenocarcinoma cells by 81 ± 15%	Biomark Res. 2021 Sep 6;9(1):69.
PC9, H1975, HCC827, HCC2935	500 nM	21 days	RNA-seq analysis revealed significant changes in gene expression regulation in osimertinib DTPs, particularly upregulation of EMT-related pathways and downregulation of cell cycle and MAPK signaling pathways.	NPJ Precis Oncol. 2022 Dec 27;6(1):95.
PC9, H1975, HCC827, HCC2935	500 nM	24 days	ATAC-seq analysis revealed significant changes in chromatin accessibility in osimertinib DTPs, particularly upregulation of EMT-related pathways and downregulation of tyrosine kinase signaling pathways.	NPJ Precis Oncol. 2022 Dec 27;6(1):95.
PC9 cells	2 μM	9 days	To evaluate the role of YAP in drug tolerance, an increase in YAP nuclear localization was observed.	Nat Commun. 2024 May 3;15(1):3741.
H1975 cells	2 μM	9 days	To evaluate the role of YAP in drug tolerance, an increase in YAP nuclear localization was observed.	Nat Commun. 2024 May 3;15(1):3741.

Cell Line

Concentration

Treated Time

Description

References

PC9

1uM

24 h

To evaluate the effect of Osimertinib on EGFR, AKT, and ERK signaling pathways, results showed that in resistant cells, EGFR signaling was suppressed, but ERK and AKT signaling was enhanced, and apoptosis was reduced.

Nat Med. 2019 Jan;25(1):111-118.

H1975

1uM

24 h

Nat Med. 2019 Jan;25(1):111-118.

HCC827

0.01–2 µM

3 days

To observe the acute treatment response of HCC827 cells to Osimertinib, it was found that a subpopulation of tumor cells survived the initial treatment.

Nat Metab. 2019 Apr;1(4):460-474.

HCC827

160 nM

2–3 weeks

To observe the survival of HCC827 cells under continuous exposure to 160 nM Osimertinib, it was found that a small percentage of cells could survive for more than 2-3 weeks.

Nat Metab. 2019 Apr;1(4):460-474.

H1975 cells

0.1 μM

72 h

Osimertinib inhibited the growth of H1975 cells by 28 ± 13%

Biomark Res. 2021 Sep 6;9(1):69.

EGFR-mutant lung adenocarcinoma cells

0.1 μM

72 h

Osimertinib inhibited the growth of EGFR-mutant lung adenocarcinoma cells by 81 ± 15%

Biomark Res. 2021 Sep 6;9(1):69.

PC9, H1975, HCC827, HCC2935

500 nM

21 days

RNA-seq analysis revealed significant changes in gene expression regulation in osimertinib DTPs, particularly upregulation of EMT-related pathways and downregulation of cell cycle and MAPK signaling pathways.

NPJ Precis Oncol. 2022 Dec 27;6(1):95.

PC9, H1975, HCC827, HCC2935

500 nM

24 days

ATAC-seq analysis revealed significant changes in chromatin accessibility in osimertinib DTPs, particularly upregulation of EMT-related pathways and downregulation of tyrosine kinase signaling pathways.

NPJ Precis Oncol. 2022 Dec 27;6(1):95.

PC9 cells

2 μM

9 days

To evaluate the role of YAP in drug tolerance, an increase in YAP nuclear localization was observed.

Nat Commun. 2024 May 3;15(1):3741.

H1975 cells

2 μM

9 days

To evaluate the role of YAP in drug tolerance, an increase in YAP nuclear localization was observed.

Nat Commun. 2024 May 3;15(1):3741.

Osimertinib mesylate/奥希替尼甲磺酸盐动物实验

Species Mice Mice BALB/cA nude mice Mice Mice	Animal Model PC9-OR cell xenograft model Non-small cell lung cancer xenograft model NCI-H1975 xenograft model H1975 xenograft model Orthotopic NSCLC model	Administration	Dosage	Frequency	Description	References
Mice	PC9-OR cell xenograft model	Oral	5mg/kg	Once daily for 71 days	To evaluate the effect of Osimertinib in combination with Aurora kinase inhibitor MLN8237 on tumor growth, results showed that the combination significantly suppressed tumor growth.	Nat Med. 2019 Jan;25(1):111-118.
Mice	Non-small cell lung cancer xenograft model	Oral	5 mg/kg	Once daily for 95 days	To investigate the resistance mechanisms of Osimertinib in EGFR L858R and T790M mutant non-small cell lung cancer xenograft models. The results showed that continuous Osimertinib treatment led to the emergence of BRAF G7V and PIK3C2A A86fs mutations, along with a decrease in the frequency of EGFR L858R and T790M mutations, resulting in drug resistance.	Cancer Commun (Lond). 2018 May 9;38(1):19
BALB/cA nude mice	NCI-H1975 xenograft model	Oral	1, 5, 10 mg/kg	Once daily for 21 days	To evaluate the in vivo antitumor activity of ASK120067 in the NCI-H1975 xenograft model, the results showed that ASK120067 dose-dependently inhibited tumor growth and caused significant tumor shrinkage at the dose of 10 mg/kg.	Mol Cancer. 2020 May 13;19(1):90.
Mice	H1975 xenograft model	Orally	5 mg/kg	5 days a week for 3 consecutive weeks	To evaluate the effect of Osimertinib on tumor volume in vivo, a significant reduction in tumor volume was observed.	Nat Commun. 2024 May 3;15(1):3741.
Mice	Orthotopic NSCLC model	Oral	3.125 mg/kg	Once daily, 5/7 days	To evaluate the effect of osimertinib in combination with AZ1366 on tumor growth and survival, results showed that the combination treatment did not significantly improve survival.	Clin Cancer Res. 2017 Mar 15;23(6):1531-1541.

Species

Mice Mice BALB/cA nude mice Mice Mice

Animal Model

PC9-OR cell xenograft model Non-small cell lung cancer xenograft model NCI-H1975 xenograft model H1975 xenograft model Orthotopic NSCLC model

Administration

Dosage

Frequency

Description

References

Mice

PC9-OR cell xenograft model

Oral

5mg/kg

Once daily for 71 days

To evaluate the effect of Osimertinib in combination with Aurora kinase inhibitor MLN8237 on tumor growth, results showed that the combination significantly suppressed tumor growth.

Nat Med. 2019 Jan;25(1):111-118.

Mice

Non-small cell lung cancer xenograft model

Oral

5 mg/kg

Once daily for 95 days

To investigate the resistance mechanisms of Osimertinib in EGFR L858R and T790M mutant non-small cell lung cancer xenograft models. The results showed that continuous Osimertinib treatment led to the emergence of BRAF G7V and PIK3C2A A86fs mutations, along with a decrease in the frequency of EGFR L858R and T790M mutations, resulting in drug resistance.

Cancer Commun (Lond). 2018 May 9;38(1):19

BALB/cA nude mice

NCI-H1975 xenograft model

Oral

1, 5, 10 mg/kg

Once daily for 21 days

To evaluate the in vivo antitumor activity of ASK120067 in the NCI-H1975 xenograft model, the results showed that ASK120067 dose-dependently inhibited tumor growth and caused significant tumor shrinkage at the dose of 10 mg/kg.

Mol Cancer. 2020 May 13;19(1):90.

Mice

H1975 xenograft model

Orally

5 mg/kg

5 days a week for 3 consecutive weeks

To evaluate the effect of Osimertinib on tumor volume in vivo, a significant reduction in tumor volume was observed.

Nat Commun. 2024 May 3;15(1):3741.

Mice

Orthotopic NSCLC model

Oral

3.125 mg/kg

Once daily, 5/7 days

To evaluate the effect of osimertinib in combination with AZ1366 on tumor growth and survival, results showed that the combination treatment did not significantly improve survival.

Clin Cancer Res. 2017 Mar 15;23(6):1531-1541.

Osimertinib mesylate/奥希替尼甲磺酸盐动物研究

Dose

Mice: 5 mg/kg, 10 mg/kg^[1] (p.o.) Rat: 200 mg/kg^[1] (p.o.)

Administration

p.o.

Pharmacokinetics

Animal	Dogs^[3]
Dose	1 mg/kg (i.v.) 2 mg/kg (p.o.)
Administration	i.v. p.o.
F	115% (p.o.)
V_d	18.2 L/kg (i.v.)
T_1/2	10.3 h (i.v.) 13.1 h (p.o.)
T_max	2 h (p.o.)
CL	1.28 L/h/kg (i.v.)
C_max	195 nmol/L (i.v.) 201 nmol/L (p.o.)
AUC_0→t	1550 nmol·h/L (i.v.) 3740 nmol·h/L (p.o.)

Osimertinib mesylate/奥希替尼甲磺酸盐参考文献

Osimertinib mesylate/奥希替尼甲磺酸盐实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

1.68mL

0.34mL

0.17mL

8.39mL

1.68mL

0.84mL

16.79mL

3.36mL

1.68mL

Osimertinib mesylate/奥希替尼甲磺酸盐技术信息

CAS号	1421373-66-1
分子式	C₂₉H₃₇N₇O₅S
分子量	595.71
SMILES Code	C=CC(NC1=CC(NC2=NC=CC(C3=CN(C)C4=C3C=CC=C4)=N2)=C(OC)C=C1N(CCN(C)C)C)=O.CS(=O)(O)=O
MDL No.	MFCD28137994

别名	AZD-9291 甲磺酸盐 ;AZD-9291 mesylate; Mereletinib mesylate
运输	蓝冰
InChI Key	FUKSNUHSJBTCFJ-UHFFFAOYSA-N
Pubchem ID	78357807

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, 2-8°C

溶解方案

细胞实验：

DMSO: 12 mg/mL(20.14 mM)，配合低频超声，并水浴加热至45℃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

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

Osimertinib mesylate/奥希替尼甲磺酸盐 {[allProObj[0].p_purity_real_show]}

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Osimertinib mesylate/奥希替尼甲磺酸盐质控信息

Osimertinib mesylate/奥希替尼甲磺酸盐生物活性

Osimertinib mesylate/奥希替尼甲磺酸盐细胞实验

Osimertinib mesylate/奥希替尼甲磺酸盐动物实验

Osimertinib mesylate/奥希替尼甲磺酸盐动物研究

Osimertinib mesylate/奥希替尼甲磺酸盐参考文献

Osimertinib mesylate/奥希替尼甲磺酸盐实验方案

Osimertinib mesylate/奥希替尼甲磺酸盐技术信息

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Osimertinib mesylate/奥希替尼甲磺酸盐技术信息