A-196

发表于2025年12月31日由上海金畔生物科技有限公司

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

A-196 纯度: 99.73%

A-196 是一种有效的选择性的 SUV420H1 和 SUV420H2 抑制剂，其 IC₅₀ 值分别为 25 nM 和 144 nM。A-196 以底物竞争性方式抑制 SUV4-20，也是一种 SUV4-20 的化学探针，用于研究组蛋白甲基转移酶在基因组完整性中的作用。

A-196 Chemical Structure

CAS No. : 1982372-88-2

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Free Sample (0.1-0.5 mg)		Apply now
10 mM * 1 mL in DMSO	￥869	In-stock
5 mg	￥1100	In-stock
10 mg	￥1800	In-stock
50 mg	￥5900	In-stock
100 mg	￥9500	In-stock
200 mg		询价
500 mg		询价

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A-196 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Epigenetics Compound Library
Histone Modification Research Compound Library
Anti-Cancer Compound Library
Reprogramming Compound Library
Chemical Probe Library
Anti-Blood Cancer Compound Library

生物活性

A-196 is a potent and selective inhibitor of SUV420H1 and SUV420H2 with IC₅₀ values of 25 nM and 144 nM, respectively. A-196 inhibits SUV4-20 biochemically in a substrate-competitive manner. A-196 represents a first-in-class chemical probe of SUV4-20 to investigate the role of histone methyltransferases in genomic integrity^[1].

IC₅₀ & Target

IC50: 25 nM (SUV420H1) and 144 nM (SUV420H2)^[1].

体外研究
(In Vitro)

A-196 (0-5 μM; 48 hours; U2OS cells) treatment results in an increase in H4K20me1 (EC₅₀ value of 735 nM) and a decrease in both H4K20me2 and H4K20me3 (EC₅₀ values of 262 and 370 nM, respectively)^[1].
A-196 (10 μM; 72 hours; Wild-type, Suv4-20h double knockout and inhibitortreated mouse embryonic fibroblast cells) inhibits both SUV4-20 enzymes in cells in multiple tissue types without overt toxicity^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:	U2OS cells
Concentration:	0 μM, 0.075 μM, 0.15 μM, 0.3 μM, 0.6 μM, 1.25 μM, 2.5 μM, 5 μM
Incubation Time:	48 hours
Result:	Increased in H4K20me1 and decreased in both H4K20me2 and H4K20me3.

分子量

359.25

Formula

C₁₈H₁₆Cl₂N₄

CAS 号

1982372-88-2

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : ≥ 31 mg/mL (86.29 mM)

* “≥” means soluble, but saturation unknown.

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.7836 mL	13.9179 mL	27.8358 mL
5 mM	0.5567 mL	2.7836 mL	5.5672 mL
10 mM	0.2784 mL	1.3918 mL	2.7836 mL

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用；以下溶剂前显示的百
分比是指该溶剂在您配制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

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 1 mg/mL (2.78 mM); Clear solution

此方案可获得 ≥ 1 mg/mL (2.78 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 10.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: 1 mg/mL (2.78 mM); Suspended solution; Need ultrasonic

此方案可获得 1 mg/mL (2.78 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

以 1 mL 工作液为例，取 100 μL 10.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
3.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 1 mg/mL (2.78 mM); Clear solution

此方案可获得 ≥ 1 mg/mL (2.78 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 10.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Bromberg KD, et al. The SUV4-20 inhibitor A-196 verifies a role for epigenetics in genomic integrity. Nat Chem Biol. 2017 Mar;13(3):317-324.

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LPM4870108

发表于2025年12月30日由上海金畔生物科技有限公司

LPM4870108

LPM4870108 是一种有效且具有口服活性的泛 Trk (WT/MT) 抑制剂，对 TrkC，TrkA，TrkA^G595R 和 TrkA^G667C 的 IC₅₀ 分别为 0.2 nM、2.4 nM、3.5 nM 和 2.3 nM。LPM4870108 显示了对 Trk 的选择性超过 ALK (IC₅₀=182 nM)。LPM4870108 具有抗肿瘤活性。

LPM4870108 Chemical Structure

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生物活性

LPM4870108 is a potent and orally active pan-Trk (WT and MT) inhibitor, with IC₅₀s of 0.2 nM, 2.4 nM, 3.5 nM and 2.3 nM for TrkC, TrkA, TrkA^G595R and TrkA^G667C, respectively. LPM4870108 shows selectivity for Trk over ALK (IC₅₀=182 nM). LPM4870108 exhibits anti-tumor activity^[1]^[2].

IC₅₀ & Target^[1]

TrkC

0.2 nM (IC₅₀)

TrkA

2.4 nM (IC₅₀)

体外研究
(In Vitro)

LPM4870108 (compound 10) inhibits the activities of TrkA, TrkB, and TRC with high selectivity at 0.5 μM (kinase activity remaining, <10%) and slightly inhibit the activities of ALK and ROS1 (kinase activity remaining, 10-30%)^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

LPM4870108 (compound 10) (5-20 mg/kg; p.o. once daily for 21 days) inhibits tumor growth in BaF3-NTRK xenograft tumor models^[1].
LPM4870108 (2 mg/kg; a single i.v.) exhibits terminal half-life (t_1/2) (male 0.87 h, 2.21 h), the Cl (male 19.3 mL/kg/min, female 8.19 mL/kg/min), and the AUC_0-t (male 4191 nM•h, female 10282 nM•h) in rats^[1].
LPM4870108 (10 mg/kg; a single p.o.) exhibits oral bioavailability (male 56.0%, female 61.9%), C_max (male 6384 nM, female 6628 nM) and T_max (male 0.667 h, female 0.667 h) in rats^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Mice bearing 100-200 mm³ BaF3-NTRK tumors^[1]
Dosage:	5, 10, 20 mg/kg
Administration:	P.o. once daily for 21 days
Result:	Showed slight weight loss and all animals survived at the highest dose.

Animal Model:	Sprague-Dawley rats (six males and six females)^[1]
Dosage:	2 mg/kg for i.v.; 10 mg/kg for oral (Pharmacokinetic Analysis)
Administration:	Intravenous administration and oral administration
Result:	I.v.: t_1/2 (male 0.87 h, 2.21 h), Cl (male 19.3 mL/kg/min, female 8.19 mL/kg/min), AUC_0-t (male 4191 nM•h, female 10282 nM•h). P.o.: F (male 56.0%, female 61.9%), C_max (male 6384 nM, female 6628 nM), T_max (male 0.667 h, female 0.667 h).

分子量

410.40

Formula

C₂₀H₁₉FN₆O₃

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Liu Z, et, al. Discovery of the Next-Generation Pan-TRK Kinase Inhibitors for the Treatment of Cancer. J Med Chem. 2021 Jul 22;64(14):10286-10296.

[2]. Duan S, et, al. Assessment of the toxicity and toxicokinetics of the novel potent tropomyosin receptor kinase (Trk) inhibitor LPM4870108 in rhesus monkeys. Regul Toxicol Pharmacol. 2021 Jun;122:104886.

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FD223

发表于2025年12月29日由上海金畔生物科技有限公司

FD223 纯度: 98.68%

FD223 是一种有效且选择性的磷酸肌醇3-激酶δ (PI3Kδ) 抑制剂。FD223 显示出高效价 (IC₅₀=1 nM) 和对其他异构体的良好选择性 (α、β 和 γ 的IC₅₀ 值分别为 51 nM、29 nM 和 37nM）。FD223通过抑制 p-AKT Ser473 有效抑制急性髓系白血病 (AML) 细胞系的增殖，从而导致细胞周期 G1 期阻滞。FD223 在 AML 等白血病的研究中具有潜力。

FD223 Chemical Structure

CAS No. : 2050524-24-6

规格	价格	是否有货
5 mg	￥3000	In-stock
10 mg	￥4800	In-stock
25 mg	￥9500	In-stock
50 mg	￥14500	In-stock
100 mg		询价
200 mg		询价

* Please select Quantity before adding items.

FD223 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Apoptosis Compound Library
Kinase Inhibitor Library
PI3K/Akt/mTOR Compound Library
Stem Cell Signaling Compound Library
Anti-Cancer Compound Library
Autophagy Compound Library
Anti-Aging Compound Library
Differentiation Inducing Compound Library
Oxygen Sensing Compound Library
Glycolysis Compound Library
Cytoskeleton Compound Library
Orally Active Compound Library
Anti-Breast Cancer Compound Library
Anti-Lung Cancer Compound Library
Anti-Pancreatic Cancer Compound Library
Anti-Blood Cancer Compound Library
Anti-Cancer Metabolism Compound Library
Angiogenesis Related Compound Library
Glucose Metabolism Compound Library
Anti-Liver Cancer Compound Library
Anti-Colorectal Cancer Compound Library

生物活性

FD223 is a potent and selective phosphoinositide 3-kinase delta (PI3Kδ) inhibitor. FD223 displays high potency (IC₅₀=1 nM) and good selectivity over other isoforms (IC₅₀s of 51 nM, 29 nM and 37 nM, respectively for α, β and γ). FD223 exhibits efficient inhibition of the proliferation of acute myeloid leukemia (AML) cell lines by suppressing p-AKT Ser473 thus causing G1 phase arrest during the cell cycle. FD223 has potential for the research of leukemia such as AML^[1].

IC₅₀ & Target^[1]

PI3Kδ

1 nM (IC₅₀)

PI3Kα

51 nM (IC₅₀)

PI3Kβ

29 nM (IC₅₀)

PI3Kγ

37 nM (IC₅₀)

体外研究
(In Vitro)

FD223 exhibits notable anti-proliferative activities in the p110δ-positive AML cell lines HL-60, MOLM-16, EOL-1 and KG-1, with the IC₅₀ of 2.25 μM, 0.87 μM, 2.82 μM, and 5.82 μM, respectively. FD223 shows weak anti-proliferative activity against p110δ unexpressed MM.1R cell line, with the IC50 value of 23.13 μM^[1].
FD223 (MOLM-16 cells; 0.1-5 μM; 16 hours) dose-dependently reduces phosphorylation of Akt (Ser473), which is consistent with the positive control Idelalisib, illustrating that the activity of PI3K/Akt pathway in MOLM-16 cell is blocked^[1].
FD223 (MOLM-16 cells; 24 hours; 1-5 μM) arrests the cell cycle at the G1 phase similar to that of positive control Idelalisib^[1].
FD223 (1-5 μM; 48 hours) dose-dependently induces cellular apoptosis^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Apoptosis Analysis^[1]

Cell Line:	MOLM-16 cells
Concentration:	1-5 μM
Incubation Time:	48 hours
Result:	Dose-dependently induced cellular apoptosis, which is superior to that of positive control Idelalisib.

Western Blot Analysis^[1]

Cell Line:	MOLM-16 cells
Concentration:	0.1-5 μM
Incubation Time:	16 hours
Result:	Dose-dependently reduced phosphorylation of Akt (Ser473).

体内研究
(In Vivo)

FD223 (20 and 40 mg/kg; p.o, per day for 14 consecutive days) displays potent antitumor efficacy in MOLM-16 xenograft model with the tumor volume reduction of 49% at a dose of 40 mg/kg/day (po), and shows no significant toxicity in the preliminary safety assessment^[1].
FD223 (i.v.; dose of 2 mg/kg; p.o.; 10 mg/kg rats) shows a moderate plasma clearance rate after intravenous administration with C =0.191 L•h^-1•kg^-1. In the po route, it shows a half-life (t_1/2) of 3.74 h and a Cmax of 1104 ng/mL, good oral plasma exposures (AUC_0-∞>9000 h•ng/mL) and acceptable oral bioavailability (17.6%)^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	MOLM-16 xenograft model of BALB/c nude mice^[1]
Dosage:	20 and 40 mg/kg
Administration:	P.o, per day for 14 consecutive days
Result:	Showed a dose-dependent tumor growth inhibition (TGI) of 31% for 20 mg/kg and 49% for 40 mg/kg

分子量

385.83

Formula

C₁₇H₁₂ClN₅O₂S

CAS 号

2050524-24-6

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : 100 mg/mL (259.18 mM; Need ultrasonic)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.5918 mL	12.9591 mL	25.9182 mL
5 mM	0.5184 mL	2.5918 mL	5.1836 mL
10 mM	0.2592 mL	1.2959 mL	2.5918 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.5 mg/mL (6.48 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (6.48 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: 2.5 mg/mL (6.48 mM); Suspended solution; Need ultrasonic

此方案可获得 2.5 mg/mL (6.48 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明

*以上所有助溶剂都可在 Shanghai Jinpan Biotech Co Ltd 网站选购。

参考文献

[1]. Yang C, et al. Bioisosteric replacements of the indole moiety for the development of a potent and selective PI3Kδ inhibitor: Design, synthesis and biological evaluation [published online ahead of print, 2021 Jun 21]. Eur J Med Chem. 2021;223:113661.

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Hu7691

发表于2025年12月28日由上海金畔生物科技有限公司

Hu7691

Hu7691 是一种具有口服活性的，选择性 Akt 抑制剂，对 Akt1、Akt2 和 Akt3 的 IC₅₀ 分别为 4.0 nM、97.5 nM、28 nM。Hu7691 抑制肿瘤生长并降低小鼠的皮肤毒性。

Hu7691 Chemical Structure

CAS No. : 2360523-76-6

规格		是否有货
100 mg		询价
250 mg		询价
500 mg		询价

* Please select Quantity before adding items.

生物活性

Hu7691 is an orally active, selective Akt inhibitor with IC₅₀s of 4.0 nM, 97.5 nM, 28 nM for Akt1, Akt2 and Akt3, respectively. Hu7691 inhibits tumor growth and enables decrease of cutaneous toxicity in mice^[1].

IC₅₀ & Target^[1]

Akt1

4.0 nM (IC₅₀)

Akt2

97.5 nM (IC₅₀)

Akt3

28 nM (IC₅₀)

PKA

11 nM (IC₅₀)

PKCη

629 nM (IC₅₀)

ROCK1

354 nM (IC₅₀)

RSK1

756 nM (IC₅₀)

p70S6K

229 nM (IC₅₀)

体外研究
(In Vitro)

Hu7691 displays low inhibitions against most of the kinases in the four families (AGC, TK, TKL, Lipid/Atypical; PKA, IC₅₀=11 nM; PKCη, IC₅₀=629 nM; ROCK1, IC₅₀=354 nM; RSK1, IC₅₀=756 nM; P70S6K, IC₅₀=229 nM; SGK, IC₅₀=1009 nM)^[1].
Hu7691 (2.25-36 μM; 24 hours) induces effective decrease of the phosphorylation level of Akt (S473)^[1].
B5 (10, 20, 30, 40 μM; for 72 h) exhibits low toxicity against HaCaT cells with an IC₅₀ value of 15.2 μM^[1].
Hu7691 has a significant inhibitory effect on the growth of 18 kinds of human tumor cells (U87-MG, U251, A549, HepG2, HT-29, KHOS, MDA-MB-231, PC3, SKOV3 and so on) derived from different tissues, with the IC₅₀ range of 0.6-27 μM. Hu7691 shows low antiproliferation activities against the HL7702 and HPDE6-C7 normal cells, exhibiting IC₅₀ values of 5.4 and 16.1 μM, respectively^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:	HaCaT cells
Concentration:	2.25, 4.5, 9, 18, 36 μM
Incubation Time:	24 hours
Result:	Induced effective decrease of the phosphorylation level of Akt (S473).

体内研究
(In Vivo)

Hu7691 (12.5-50 mg/kg/day; i.g.; for 22 days) shows dose-dependent tumor growth inhibition^[1].
Hu7691 (15 mg/kg; oral) has a T_1/2 of 8.68 hours, a C_max of 171.17 ng/mL and an AUC of 2820.64 ng/mL•h in rats^[1].
Hu7691 (2 mg/kg; iv) has a T_1/2 of 6.24 hours, a C_max of 207.52 ng/mL and an AUC of 532.87 ng/mL•h in rats^[1].
Hu7691 (20 mg/kg; oral) has a T_1/2 of 16.7 hours, a C_max of 905.65 ng/mL and an AUC of 36303 ng/mL•h in beagle dog (male, 40 weeks old, 8–10 kg)^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Balb/c mice (nu/nu, female, 3-4 weeks old, 20-25 g) with 786-O and KHOS xenograft^[1]
Dosage:	12.5, 25, 50 mg/kg
Administration:	Oral; once daily for 22 days
Result:	Showed dose-dependent tumor growth inhibition.

Animal Model:	SD rats (male, 8 weeks old, 250-300 g)^[1]
Dosage:	15 mg/kg (Pharmacokinetic Analysis)
Administration:	Oral
Result:	Had a T_1/2 of 8.68 hours, a C_max of 171.17 ng/mL and an AUC of 2820.64 ng/mL•h.

分子量

450.88

Formula

C₂₂H₂₂ClF₃N₄O

CAS 号

2360523-76-6

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Jinxin Che, et al. Discovery of N-((3 S,4 S)-4-(3,4-Difluorophenyl)piperidin-3-yl)-2-fluoro-4-(1-methyl-1 H-pyrazol-5-yl)benzamide (Hu7691), a Potent and Selective Akt Inhibitor That Enables Decrease of Cutaneous Toxicity. J Med Chem. 2021 Aug 26;64(16):12163-12180.

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K00546

发表于2025年12月27日由上海金畔生物科技有限公司

K00546 纯度: 98.78%

K00546 是一种有效的 CDK1 和 CDK2 抑制剂，对 CDK1/cyclin B 和 CDK2/cyclin A 的 IC₅₀ 分别为 0.6 nM 和 0.5 nM。K00546 也是一种有效的 CDC2 样激酶 1 (CLK1) 和 CLK3 抑制剂，IC₅₀ 分别为 8.9 nM 和 29.2 nM。

K00546 Chemical Structure

CAS No. : 443798-47-8

规格	价格	是否有货
10 mM * 1 mL in DMSO	￥3080	In-stock
5 mg	￥2800	In-stock
10 mg	￥4500	In-stock
50 mg	￥13000	In-stock
100 mg	￥20000	In-stock
200 mg		询价
500 mg		询价

* Please select Quantity before adding items.

K00546 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Cell Cycle/DNA Damage Compound Library
Kinase Inhibitor Library
PI3K/Akt/mTOR Compound Library
Protein Tyrosine Kinase Compound Library
Stem Cell Signaling Compound Library
Wnt/Hedgehog/Notch Compound Library
Anti-Cancer Compound Library
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生物活性

K00546 is a potent CDK1 and CDK2 inhibitor with IC₅₀s of 0.6 nM and 0.5 nM for CDK1/cyclin B and CDK2/cyclin A, respectively. K00546 is also a potent CDC2-like kinase 1 (CLK1) and CLK3 inhibitor with IC₅₀s of 8.9 nM and 29.2 nM, respectively^[1]^[2]^[3].

IC₅₀ & Target

Cdk1/cyclin B

0.6 nM (IC₅₀)

cdk2/cyclin A

0.5 nM (IC₅₀)

CLK1

8.9 nM (IC₅₀)

CLK3

29.2 nM (IC₅₀)

GSK-3

140 nM (IC₅₀)

VEGF-R2

32 nM (IC₅₀)

体外研究
(In Vitro)

K00546 binds to the SLK ATP-binding site forming three hydrogen bonds with the kinase hinge residues E109 and C111. The sulphamoyl moiety of K00546 also interacts with the main chain of L40^[1].
K00546 (compound 3n) also inhibits PKA, casein kinase-1, MAP kinase (ERK-2), calmodulin kinase, VEGF-R2, GSK-3 and PDGF-Rβ with IC₅₀ values of 5.2 μM, 2.8 μM, 1.0 μM, 8.9 μM, 0.032 μM, 0.14 μM and 1.6 μM, respectively^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

425.44

Formula

C₁₅H₁₃F₂N₇O₂S₂

CAS 号

443798-47-8

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : 100 mg/mL (235.05 mM; Need ultrasonic)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.3505 mL	11.7525 mL	23.5051 mL
5 mM	0.4701 mL	2.3505 mL	4.7010 mL
10 mM	0.2351 mL	1.1753 mL	2.3505 mL

参考文献

[1]. Ashley C W Pike, et al. Activation segment dimerization: a mechanism for kinase autophosphorylation of non-consensus sites. EMBO J. 2008 Feb 20;27(4):704-14.

[2]. Ronghui Lin, et al. 1-Acyl-1H-[1,2,4]triazole-3,5-diamine analogues as novel and potent anticancer cyclin-dependent kinase inhibitors: synthesis and evaluation of biological activities. J Med Chem. 2005 Jun 30;48(13):4208-11.

[3]. Oleg Fedorov, et al. Specific CLK inhibitors from a novel chemotype for regulation of alternative splicing. Chem Biol. 2011 Jan 28;18(1):67-76.

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JNJ-7706621

发表于2025年12月26日由上海金畔生物科技有限公司

JNJ-7706621 纯度: 99.96%

JNJ-7706621 是一种有效的 aurora kinase 抑制剂，同时能有效抑制 CDK1 和 CDK2，对 CDK1，CDK2，aurora-A 和 aurora-B 的 IC₅₀ 值分别为 9 nM，3 nM，11 nM 和 15 nM。

JNJ-7706621 Chemical Structure

CAS No. : 443797-96-4

规格	价格	是否有货
10 mM * 1 mL in DMSO	￥1215	In-stock
2 mg	￥800	In-stock
5 mg	￥1400	In-stock
10 mg	￥2500	In-stock
50 mg	￥6100	In-stock
100 mg	￥11700	In-stock
200 mg		询价
500 mg		询价

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生物活性

JNJ-7706621 is a potent aurora kinase inhibitor, and also inhibits CDK1 and CDK2, with IC₅₀s of 9 nM, 3 nM, 11 nM, and 15 nM for CDK1, CDK2, aurora-A and aurora-B, respectively^[1]^[2]^[3].

IC₅₀ & Target

CDK2/cyclinE

3 nM (IC₅₀)

cdk2/cyclin A

4 nM (IC₅₀)

Cdk1/cyclin B

9 nM (IC₅₀)

CDK3/Cyclin E

58 nM (IC₅₀)

CDK6/cyclinD1

175 nM (IC₅₀)

Cdk4/cyclin D1

253 nM (IC₅₀)

Aurora A

11 nM (IC₅₀)

Aurora B

15 nM (IC₅₀)

VEGF-R1

6400 nM (IC₅₀)

VEGF-R2

154 nM (IC₅₀)

VEGF-R3

735 nM (IC₅₀)

FGF-R1

575 nM (IC₅₀)

FGF-R2

226 nM (IC₅₀)

GSK3β

254 nM (IC₅₀)

体外研究
(In Vitro)

JNJ-7706621 shows antiproliferative activity against various human tumor cells with IC₅₀s of 284, 254, and 447 nM for HeLa, HCT116, and A375, respectively^[1]. JNJ-7706621 inhibits other centrosomal proteins such as TOG, Nek2, and TACC3 in early mitotic phase, but does not prevent localization of Aurora A to the spindle poles. Treatment of nocodazole-synchronized cells with JNJ-7706621 can override mitotic arrest by preventing spindle checkpoint signaling, resulting in failure of chromosome alignment and segregation^[2]. JNJ-7706621 shows inhibition of Aurora-A and Aurora-B but has no activity at the highest concentration tested on the Plk1 or Wee1 serine/threonine kinases. JNJ-7706621 also shows potent growth inhibition in vitro on all human cancer cell types with IC₅₀ values ranging from 112 to 514 nM^[3]. JNJ-7706621 suspensions inhibits cell viability of HeLa cells with IC₅₀s of 2.1 and 0.9 μg/mL at 24 and 48 h. The IC₅₀ of the JNJ-7706621-loaded nanoparticles are 35 and 2.7 μg/mL and the IC₅₀ of the JNJ-7706621-loaded micelles are 6.3 and 1.6 μg/mL^[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

JNJ-7706621 (100 and 125 mg/kg) is efficacious in a human tumor xenograft model under intermittent dosing regimens^[3]. JNJ-7706621 (100 mg/kg, i.p.) exhibits 95% tumor growth inhibition in A375 (human melanoma) tumor xenograft model^[1]. JNJ-7706621-loaded micelles inhibit tumor growth, and delay the tumor growth more efficiently than the control JNJ-7706621 suspension^[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

394.36

Formula

C₁₅H₁₂F₂N₆O₃S

CAS 号

443797-96-4

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : ≥ 125 mg/mL (316.97 mM)

* “≥” means soluble, but saturation unknown.

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.5358 mL	12.6788 mL	25.3575 mL
5 mM	0.5072 mL	2.5358 mL	5.0715 mL
10 mM	0.2536 mL	1.2679 mL	2.5358 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.08 mg/mL (5.27 mM); Clear solution

此方案可获得 ≥ 2.08 mg/mL (5.27 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.08 mg/mL (5.27 mM); Clear solution

此方案可获得 ≥ 2.08 mg/mL (5.27 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Huang S, et al. Synthesis and evaluation of N-acyl sulfonamides as potential prodrugs of cyclin-dependent kinase inhibitor JNJ-7706621. Bioorg Med Chem Lett. 2006 Jul 15;16(14):3639-41. Epub 2006 May 6.

[2]. Matsuhashi A, et al. Growth suppression and mitotic defect induced by JNJ-7706621, an inhibitor of cyclin-dependent kinases and aurora kinases. Curr Cancer Drug Targets. 2012 Jul;12(6):625-39.

[3]. Emanuel S, et al. The in vitro and in vivo effects of JNJ-7706621: a dual inhibitor of cyclin-dependent kinases and aurora kinases. Cancer Res. 2005 Oct 1;65(19):9038-46.

[4]. Danhier F, et al. Active and passive tumor targeting of a novel poorly soluble cyclin dependent kinase inhibitor, JNJ-7706621. Int J Pharm. 2010 Jun 15;392(1-2):20-8.

Kinase Assay ^[4]	To identify compounds that inhibit CDK1 kinase activity, a screening method is developed using the CDK1/cyclin B complex to phosphorylate a biotinylated peptide substrate containing the consensus phosphorylation site for histone H1, which is phosphorylatedin vivo by CDK1. Inhibition of CDK1 activity is measured by observing a reduced amount of ³³P-g-ATP incorporation into the immobilized substrate in streptavidin-coated 96-well scintillating microplates. CDK1 enzyme is diluted in 50 mM Tris-HCl (pH 8), 10 mM MgCl₂, 0.1 mM Na₃VO₄, 1 mM DTT, 1% DMSO, 0.25 AM peptide, 0.1 ACi per well ³³P-g-ATP (2,000-3,000 Ci/mmol), and 5 AM ATP in the presence or absence of various concentrations of test compound and incubated at 30°C for 1 hour. The reaction is terminated by washing with PBS containing 100 mM EDTA and plates are counted in a scintillation counter. Linear regression analysis of the percent inhibition by test compound is used to determine IC₅₀ values. The Aurora kinase assays are done with 10 AM ATP and a peptide containing a dual repeat of the kemptide phosphorylation motif. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay ^[3]	HeLa cells are seeded in 96-well plates at the density of 2500 viable cells per well. The cells are then incubated with a suspension of JNJ-7706621, JNJ-7706621-loaded micelles and nanoparticles (JNJ-7706621 concentrations of 0.011, 0.022, 0.11, 0.22, 1.1, 2.2, 11 and 22 μg/mL; dilutions are made in the medium) and drug-free polymeric micelles (polymers concentrations 0.3 mg/mL) and nanoparticles (polymers concentration 5 mg/mL) for 4, 24 and 48 h. The cytotoxicity is assessed using the MTT test. Absorbance is measured at 570 nm using a microplate reader. Untreated cells are taken as control with 100% viability and Triton X-100 1% is used as positive control of cytotoxicity. The results are expressed as mean values ± standard deviations of five measurements. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration ^[4]	Briefly, animals are implanted s.c. with 1 mm³ A375 tumor fragments in the hindflank. After tumors reach 62 to 126 mg, groups are pair matched. Animals are given JNJ-7706621 or vehicle control starting on day 1. The tumor growth delay method is followed where each animal is euthanized when its neoplasm reached a predetermined size of 2.0 g. All statistical analyses are conducted using unpaired t tests at a P level of 0.05 (two tailed). 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献	[1]. Huang S, et al. Synthesis and evaluation of N-acyl sulfonamides as potential prodrugs of cyclin-dependent kinase inhibitor JNJ-7706621. Bioorg Med Chem Lett. 2006 Jul 15;16(14):3639-41. Epub 2006 May 6. [2]. Matsuhashi A, et al. Growth suppression and mitotic defect induced by JNJ-7706621, an inhibitor of cyclin-dependent kinases and aurora kinases. Curr Cancer Drug Targets. 2012 Jul;12(6):625-39. [3]. Emanuel S, et al. The in vitro and in vivo effects of JNJ-7706621: a dual inhibitor of cyclin-dependent kinases and aurora kinases. Cancer Res. 2005 Oct 1;65(19):9038-46. [4]. Danhier F, et al. Active and passive tumor targeting of a novel poorly soluble cyclin dependent kinase inhibitor, JNJ-7706621. Int J Pharm. 2010 Jun 15;392(1-2):20-8.

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Uzansertib(Synonyms: INCB053914)

发表于2025年12月26日由上海金畔生物科技有限公司

Uzansertib (Synonyms: INCB053914)

Uzansertib (INCB053914) 是一种具有口服活性的，ATP 竞争性泛-PIM 激酶抑制剂，对于 PIM1，PIM2 和 PIM3 的 IC₅₀ 分别为 0.24 nM，30 nM 和 0.12 nM。Uzansertib 对多种血液肿瘤细胞系具有广泛的抗增殖活性。

Uzansertib Chemical Structure

CAS No. : 1620012-39-6

规格		是否有货
100 mg		询价
250 mg		询价
500 mg		询价

* Please select Quantity before adding items.

Uzansertib 的其他形式现货产品:

Uzansertib phosphate

生物活性

Uzansertib (INCB053914) is an orally active, ATP-competitive pan-PIM kinase inhibitor with IC₅₀s of 0.24 nM, 30 nM, 0.12 nM for PIM1, PIM2, PIM3, respectively. Uzansertib has broad anti-proliferative activity against a variety of hematologic tumor cell lines^[1].

IC₅₀ & Target^[1]

PIM1

0.24 nM (IC₅₀)

PIM2

30 nM (IC₅₀)

PIM3

0.12 nM (IC₅₀)

体外研究
(In Vitro)

Uzansertib inhibits proliferation in all multiple myeloma (MM) cell lines tested, with mean GI₅₀ values ranging from 13.2 nM to 230.0 nM in AML, MM, DLBCL, MCL, and T-ALL cell lines^[1].
Uzansertib (0.1, 0.3, 1, 3, 10, 30, 100, 300, 1000 nM) inhibits the phosphorylation of downstream PIM kinase substrates (p70S6K/S6 and 4E-BP1) in a dose-dependent manner in MOLM-16 (AML), Pfeiffer (DLBCL), and KMS-12-PE/BM (MM) cell lines^[1].
PIM kinase-mediated phosphorylation of BAD in MOLM-16 and KMS-12-BM cells is particularly sensitive to inhibition by Uzansertib (mean IC₅₀, 4 nM and 27 nM, respectively)^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

Uzansertib (25-100 mg/kg; PO; twice a day; for 15 days) inhibits tumor growth in a dose-dependent manner in mice bearing MOLM-16 (AML) or KMS-12-BM (MM) ^[1].
Uzansertib demonstrates a dose-dependent inhibition of BAD phosphorylation relative to vehicle at 4 hours post dose (MOLM-16 tumors, IC₅₀=70 nM; KMS-12-BM tumors, IC₅₀=145 nM) ^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Female immune compromised (severe combined immunodeficiency [SCID]) mice (5-9 weeks of age) bearing MOLM-16 (AML) or KMS-12-BM (MM)^[1]
Dosage:	25, 50, 75, 100 mg/kg
Administration:	PO; twice a day; for 15 days
Result:	Inhibited tumor growth in a dose-dependent manner in mice.

分子量

513.51

Formula

C₂₆H₂₆F₃N₅O₃

CAS 号

1620012-39-6

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Koblish H, et al. Preclinical characterization of INCB053914, a novel pan-PIM kinase inhibitor, alone and in combination with anticancer agents, in models of hematologic malignancies. PLoS One. 2018 Jun 21;13(6):e0199108.

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SL327

发表于2025年12月25日由上海金畔生物科技有限公司

SL327 纯度: ≥98.0%

SL327 抑制 MEK1 和 MEK2，IC₅₀ 分别为 180 nM 和 220 nM。

SL327 Chemical Structure

CAS No. : 305350-87-2

规格	价格	是否有货
Free Sample (0.1-0.5 mg)		Apply now
10 mM * 1 mL in DMSO	￥550	In-stock
5 mg	￥500	In-stock
10 mg	￥884	In-stock
50 mg	￥3100	In-stock
100 mg		询价
200 mg		询价

* Please select Quantity before adding items.

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生物活性

SL327 inhibits MEK1 and MEK2, with IC₅₀ values of 180 nM and 220 nM, respectively.

IC₅₀ & Target^[1]

MEK1

180 nM (IC₅₀)

MEK2

220 nM (IC₅₀)

体外研究
(In Vitro)

The specificity of SL327 for MEK is investigated. Kinase activity is assessed by measuring the incorporation of [32P]phosphate during phosphorylation of substrate peptides specific for each kinase. Although SL327 inhibits MEK with an IC₅₀ of 0.27 μM, 10 μM SL327 has no significant effect on PKA, CaMKII, or PKC^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

SL327, which crosses the blood-brain barrier, is administered intraperitoneally at several concentrations to animals prior to cue and contextual fear conditioning. Administration of SL327 completely blocks contextual fear conditioning and significantly attenuates cue learning when measure 24 hr after training. Animals treated with SL327 exhibit significant attenuation of water maze learning; they take significantly longer to find a hidden platform compared with vehicle-treated controls and also fail to use a selective search strategy during subsequent probe trials in which the platform is removed. Mice are injected with various concentrations of SL327 (10, 30, 50 mg/kg i.p.), and 1 hr later their hippocampi are removed and assayed for activated MAPK. SL327 attenuates phosphorylated MAPK levels in a dose-dependent manner. Administration of 10, 30, or 50 mg/kg SL327 significantly attenuates p42 phospho-MAPK levels (F=20.90, P<0.0001;10 mg/kg SL327 vs. vehicle, P<0.05, and 30 and 50 mg/kg SL327 vs. vehicle, P<0.001). Injection with 30 or 50 mg/kg SL327 also significantly reduces p44 phospho-MAPK levels (F=5.627, P<0.005;30 mg/kg vs. vehicle, P<0.05, and 50 mg/kg SL327 vs. vehicle, P<0.01)^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

335.35

Formula

C₁₆H₁₂F₃N₃S

CAS 号

305350-87-2

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : 68 mg/mL (202.77 mM; Need ultrasonic)

Ethanol : 0.1 mg/mL (0.30 mM; Need ultrasonic and warming)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.9820 mL	14.9098 mL	29.8196 mL
5 mM	0.5964 mL	2.9820 mL	5.9639 mL
10 mM	0.2982 mL	1.4910 mL	2.9820 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.5 mg/mL (7.45 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (7.45 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.5 mg/mL (7.45 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (7.45 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
3.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.5 mg/mL (7.45 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (7.45 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Cheng Y, et al. Current Development Status of MEK Inhibitors. Molecules. 2017 Sep 26;22(10). pii: E1551.

[2]. Selcher JC, et al. A necessity for MAP kinase activation in mammalian spatial learning. Learn Mem. 1999 Sep-Oct;6(5):478-90.

Kinase Assay ^[2]	Protein kinase assays are performed. All kinase assays are started by adding enzyme to a mixture that included [γ-³²P]ATP and substrate. This mixture is then incubated at 30°C or 37°C for 10 min. The reaction is stopped by spotting aliquots of the reaction mixture onto Whatman P-81 phosphocellulose filter paper. The papers are then washed in 150 mM H₃PO₄, dried, and subjected to scintillation counting. The catalytic subunit of PKA is assayed by measuring [³²P]phosphate incorporation into the substrate Kemptide (100 μM). The activity of CaMKII is determined by measuring phosphorylation of the synthetic peptide Autocamtide (100 μM) in the presence of 100 μM Calcium and 10 μg/mL Calmodulin. A synthetic peptide analog of a fragment of neurogranin, NG_(28-43) (10 μM) is used as a specific substrate for the catalytic subunit of PKC. In all cases, substrate phosphorylation was linear with respect to time and enzyme concentration^[2]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration ^[2]	Mice^[2] Adult male 129S3/SvImJ mice are used. In the 1×-pairing paradigm of cue and contextual fear conditioning, animals are placed in the fear conditioning apparatus for 3 min, then a 30-sec acoustic conditioned stimulus (CS; white noise, 80 dB) is delivered. During the last second of the CS, a 1-sec shock unconditioned stimulus (US; 0.5 mA) is applied to the grid floor. To assess contextual learning, the animals are returned to the training context 24 hr post-training, and freezing behavior is scored for 5 min. To assess cue learning, the animals are placed in a different context (novel odor, lighting, cage floor, and visual cues) following contextual testing. Baseline behavior is measured for 3 min in the novel context (Pre-CS), then the tone is presented for 3 min. Freezing behavior is assessed with a time sampling procedure whereby the animal was observed for ~1 sec every 5 sec. The experimenter is blind to drug treatment. Animals are injected with either vehicle (2 mL/kg, 100% DMSO) or SL327 (10, 30, and 50 mg/kg; at 2 mL/kg, dissolved in 100% DMSO) intraperitoneally 1 hr before training^[2]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献	[1]. Cheng Y, et al. Current Development Status of MEK Inhibitors. Molecules. 2017 Sep 26;22(10). pii: E1551. [2]. Selcher JC, et al. A necessity for MAP kinase activation in mammalian spatial learning. Learn Mem. 1999 Sep-Oct;6(5):478-90.

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CYH33 methanesulfonate

发表于2025年12月24日由上海金畔生物科技有限公司

CYH33 methanesulfonate

CYH33 methanesulfonate 是一种具有口服活性的，高选择性 PI3Kα 抑制剂，对 α/β/δ/γ 亚型的 IC₅₀ 分别为 5.9 nM/598 nM/78.7 nM/225 nM。CYH33 methanesulfonate 抑制 Akt 和 ERK 的磷酸化，并显着诱导乳腺癌和非小细胞肺癌 (NSCLC) 细胞 G1 期阻滞。CYH33 methanesulfonate 具有有效的抗实体瘤的活性。

CYH33 methanesulfonate Chemical Structure

CAS No. : 1494684-33-1

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10 mg	￥14800	询问价格 & 货期

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生物活性

CYH33 methanesulfonate is an orally active, highly selective PI3Kα inhibitor with IC₅₀s of 5.9 nM/598 nM/78.7 nM/225 nM against α/β/δ/γ isoform, respectively. CYH33 methanesulfonate inhibits phosphorylation of Akt, ERK and induces significant G1 phase arrest in breast cancer cells and non-small cell lung cancer (NSCLC) cells. CYH33 methanesulfonate has potent activity against solid tumors^[1]^[2]^[3].

IC₅₀ & Target^[1]

PI3Kα

5.9 nM (IC₅₀)

PI3Kβ

598 nM (IC₅₀)

PI3Kδ

78.7 nM (IC₅₀)

PI3Kγ

225 nM (IC₅₀)

体外研究
(In Vitro)

CYH33 methanesulfonate inhibits cell proliferation with IC₅₀s below 1 μM in 56% (18/32) of the breast cancer cell lines^[2].
CYH33 (0.012-1 μM; for 24 hours) methanesulfonate significantly arrests T47D and MCF7 cells in G1 phase in a concentration-dependent manner^[2].
CYH33 (4-1000 nM; 1 hour) methanesulfonate concurrently inhibits phosphorylation of ERK and Akt in both T47D and MCF7 cells^[2].
CYH33 (0.11-1 μM; 24 hours) methanesulfonate fails to induce apoptosis in MCF7 and MDA-MB-231 cells^[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cycle Analysis^[2]

Cell Line:	Sensitive T47D, MCF7 and resistant MDA-MB-231 cells
Concentration:	0.012, 0.037, 0.11, 0.33, 1 μM
Incubation Time:	For 24 hours
Result:	Arrested T47D and MCF7 cells in G1 phase in a concentration-dependent manner, accompanied with concomitant reduced cell population in S phase. Had little effect on cell cycle distribution in resistant MDA-MB-231 cells.

Western Blot Analysis^[2]

Cell Line:	Sensitive T47D, MCF7 and resistant MDA-MB-231 cells
Concentration:	4, 12, 37, 111, 333, 1000 nM
Incubation Time:	1 hour
Result:	Concurrently inhibited phosphorylation of ERK and Akt in both T47D and MCF7 cells, whereas it had little effect on phosphorylated ERK (pERK) in MDA-MB-231 cells up to 1 μM.

体内研究
(In Vivo)

CYH33 (2-20 mg/kg; oral; once a day for 21 days) methanesulfonate potently restrains tumor growth in mice bearing human breast cancer cell xenografts^[2].
Single administration of CYH33 (20 mg/kg; oral) methanesulfonate significantly down-regulates the level of phosphorylated Akt in tumor tissues, demonstrating the suppression of PI3K signaling in nude mice^[2].
CYH33 (10 mg/kg; oral; once a day for 18-d or 20-d respectively) methanesulfonate delays the restoration of blood glucose and area under the curve (AUC) of blood glucose increased upon CYH33 treatment in T47D xenografts and R26-Pik3ca^H1047R;MMTV-Cre mice^[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	SCID mice aged 4-6 weeks bearing human breast cancer T47D xenografts^[2]
Dosage:	2, 5, 10, 20 mg/kg
Administration:	Oral; once a day for 21 days
Result:	Displayed marginal inhibitory effect on the tumor growth at lower doses (2 and 5 mg/kg) and significantly attenuated tumor growth at the dose of 10 or 20 mg/kg, yielding T/C values of 58.36% and 49.42% respectively.

分子量

694.70

Formula

C₂₅H₃₃F₃N₈O₈S₂

CAS 号

1494684-33-1

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Haoyue Xiang, et al. Abstract LB-268: Discovery of clinical candidate methyl (5-(6-((4-(methylsulfonyl)piperazin-1-yl)methyl)-4-morpholinopyrrolo[2,1-f][1,2,4]triazin-2-yl)-4-(trifluoromethyl)pyridin-2-yl)carbamate (CYH33) : A highly potent and selective PI3K alpha inhibitor for the treatment of advanced solid tumors. AACR Annual Meeting 2018; April 14-18, 2018

[2]. Xue-Ling Liu, et al. Decrease in Phosphorylated ERK Indicates the Therapeutic Efficacy of a Clinical PI3Kα-selective Inhibitor CYH33 in Breast Cancer. Cancer Lett. 2018 Oct 1;433:273-282.

[3]. Yuxiang Wang, et al. Simultaneous inhibition of PI3Kα and CDK4/6 synergistically suppresses KRAS-mutated non-small cell lung cancer. Cancer Biol Med. 2019 Feb;16(1):66-83.

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SEL24-B489

发表于2025年12月23日由上海金畔生物科技有限公司

SEL24-B489

SEL24-B489 是有效的、I 型的、口服有效的、PIM 和 FLT3-ITD 的双抑制剂，其对PIM1、PIM2 和 PIM3 的 K_d 值分别为 2 nM、2 nM、和 3 nM。

SEL24-B489 Chemical Structure

CAS No. : 1616359-00-2

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生物活性

SEL24-B489 is a potent, type I, orally active, dual PIM and FLT3-ITD inhibitor, with K_d values of 2 nM for PIM1, 2 nM for PIM2 and 3 nM for PIM3, respectively^[1].

IC₅₀ & Target^[1]

PIM1

2 nM (Kd)

PIM2

2 nM (Kd)

PIM3

3 nM (Kd)

FLT3-ITD

体外研究
(In Vitro)

In MOLM-13 and to a lesser extent in MV4-11 cells, a dose-dependent disruption of cell cycle with especially pronounced depletion of the S phase after treatment with SEL24-B489, accompanied by PARP cleavage and apoptosis was observed^[1].
SEL24-B489 causes a profound inhibition of S6 (S^235/236), but has little effect on PI3K/mTOR signaling^[1].
SEL24-B489 inhibits STAT5 (Ser⁷²⁶) and reduced expression of MCL1, whereas none of the selective inhibitors altered c-MYC abundance or induced PARP cleavage^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:	AZD1208, AC220 and AraC in AML cell lines.
Concentration:	0-10 μM.
Incubation Time:	72 h.
Result:	Decreased viability.

体内研究
(In Vivo)

SEL24-B489 (25-100 mg/kg, orally) exhibited activity in AML in vivo models^[1].
SEL24-B489 induces apoptosis of DLBCL cell lines in low/sub-micromolar concentrations and exhibits activity in a xenograft model^[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	SCID/beige mice bearing MV-4-11 tumors (FLT3-ITD+)^[1].
Dosage:	50, 75 and 100 mg/kg.
Administration:	Orally, twice daily.
Result:	Marked dose – dependent tumor reduction (67%, 74% and 82% tumor growth inhibition (TGI) for 50, 75 and 100 mg/kg daily doses, respectively).

分子量

446.14

Formula

C₁₅H₁₈Br₂N₄O₂

CAS 号

1616359-00-2

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Wojciech Czardybon, A novel, dual pan-PIM/FLT3 inhibitor SEL24 exhibits broad therapeutic potential in acute myeloid leukemia. Oncotarget. 2018 Mar 30;9(24):16917-16931.

[2]. Ewa Jablonska, et al. A Novel Pan-PIM Kinase Inhibitor, SEL24-B489, Induces Apoptosis and Inhibits Proliferation of Diffuse Large B-Cell Lymphoma Cells through Inhibition of Protein Translation and Attenuation of Myc and NFkB Activity. Blood (2015) 126 (23): 706.

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Famitinib(Synonyms: 法米替尼; SHR1020)

发表于2025年12月23日由上海金畔生物科技有限公司

Famitinib (Synonyms: 法米替尼; SHR1020)

Famitinib (SHR1020) 是一种有效的，具有口服活性的多靶点激酶抑制剂，抑制 c-kit, VEGFR-2 和 PDGFRβ 的活性，IC₅₀ 值分别为 2.3 nM、4.7 nM 和 6.6 nM。Famitinib具有抗肿瘤活性。且诱导细胞凋亡 (apoptosis)。

Famitinib Chemical Structure

CAS No. : 1044040-56-3

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生物活性

Famitinib (SHR1020), an orally active multi-targeted kinase inhibitor, inhibits the activity of c-kit, VEGFR-2 and PDGFRβ with IC₅₀ values of 2.3 nM, 4.7 nM and 6.6 nM, respectively^[1]. Famitinib exerts powerful antitumor activity in human gastric cancer cells and xenografts. Famitinib triggers apoptosis^[2].

IC₅₀ & Target^[2]

VEGFR-2

4.2 nM (IC₅₀)

PDGFRβ

6.6 nM (IC₅₀)

c-kit

2.3 nM (IC₅₀)

体外研究
(In Vitro)

Famitinib inhibits the VEGF-induced proliferation, migration and tubule formation of human umbilical vein endothelial cells, and micro-vessel spouting from matrigel-embedded rat aortic rings^[1].
Famitinib inhibits cell proliferation by inducing cell cycle arrest at the G2/M phase and causes cell apoptosis in a dose-dependent manner in gastric cancer cell lines. Famitinib (0.6-20.0 µM) inhibits gastric cancer cell growth in a dose-dependent manner^[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[3]

Cell Line:	Human gastric cancer cells BGC-823 and MGC-803
Concentration:	0, 0.6, 1.25, 2.5, 5.0, 10.0 and 20.0 µM
Incubation Time:	24, 48 and 72 hours
Result:	Inhibited cell growth in a dose-dependent manner. The IC₅₀ values in BGC-823 and MGC-803 cells were 3.6 and 3.1 µM, respectively.

体内研究
(In Vivo)

Famitinib exhibits broad and potent anti-tumor activity, leading to regression or growth arrest of various established xenografts derived from human tumor cell lines ^[1].
Famitinib significantly slows tumor growth in vivo via inhibition of angiogenesis in BGC-823 xenograft models. Famitinib (50 and 100 mg/kg;gavage) reduces xenograft growth in vivo via inhibition of angiogenesis^[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	18-20 g female BALB/c athymic nu/nu mice (age, 6–8 weeks) bearing BGC-823 xenografts^[4]
Dosage:	50 and 100 mg/kg
Administration:	Gavage, once daily for 3 weeks
Result:	Both doses exerted a similar inhibitory power, but greater toxicity was observed. Inhibited BGC-823 xenograft growth (tumor volume, 395.2 vs. 2,690.5 mm³), and animal weights were similar between groups (21.6 vs. 18.7 g).

分子量

410.48

Formula

C₂₃H₂₇FN₄O₂

CAS 号

1044040-56-3

中文名称

法米替尼

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Liguang Lou, et al. Abstract 3604: Preclinical antitumor study of famitinib, an orally available multi-targeted kinase inhibitor of VEGFR/PDGFR/c-Kit in phase I clinical trials.

[2]. Sai Ge, et al. Famitinib exerted powerful antitumor activity in human gastric cancer cells and xenografts. Oncol Lett. 2016 Sep;12(3):1763-1768.

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R547

发表于2025年12月20日由上海金畔生物科技有限公司

R547 纯度: 99.66%

R547 是一种高效、选择性的，口服有效的 ATP 竞争性的 CDK 抑制剂，对 CDK1/cyclin B、 CDK2/cyclin E 和 CDK4/cyclin D1 作用的 K_i 值分别为 2 nM、3 nM、1 nM。

R547 Chemical Structure

CAS No. : 741713-40-6

规格	价格	是否有货
Free Sample (0.1-0.5 mg)		Apply now
10 mM * 1 mL in DMSO	￥3190	In-stock
10 mg	￥2900	In-stock
50 mg	￥8500	In-stock
100 mg		询价
200 mg		询价

* Please select Quantity before adding items.

R547 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Apoptosis Compound Library
Cell Cycle/DNA Damage Compound Library
Kinase Inhibitor Library
PI3K/Akt/mTOR Compound Library
Stem Cell Signaling Compound Library
Wnt/Hedgehog/Notch Compound Library
Anti-Cancer Compound Library
Anti-Aging Compound Library
Reprogramming Compound Library
Oxygen Sensing Compound Library
Glycolysis Compound Library
Cytoskeleton Compound Library
Orally Active Compound Library
Anti-Alzheimer’s Disease Compound Library
Anti-Breast Cancer Compound Library
Anti-Pancreatic Cancer Compound Library
Anti-Blood Cancer Compound Library
Anti-Cancer Metabolism Compound Library
Neurodegenerative Disease-related Compound Library
Glucose Metabolism Compound Library
Targeted Diversity Library

生物活性

R547 is a potent, selective and orally active ATP-competitive CDK inhibitor, with K_is of 2 nM, 3 nM and 1 nM for CDK1/cyclin B, CDK2/cyclin E and CDK4/cyclin D1, respectively^[1]^[2]^[3]^[4]^[5].

IC₅₀ & Target^[1]

Cdk1/cyclin B

2 nM (Ki)

CDK2/cyclinE

3 nM (Ki)

CDK4/cyclin D

1 nM (Ki)

cdk2/cyclin A

0.1 nM (IC₅₀)

CDK2/cyclinE

0.4 nM (IC₅₀)

Cdk1/cyclin B

0.2 nM (IC₅₀)

CDK3/Cyclin E

0.8 nM (IC₅₀)

CDK5/p35

0.1 nM (IC₅₀)

cdk6/cyclin D3

4 nM (IC₅₀)

CDK7/cyclin H

171 nM (IC₅₀)

GSK-3α

46 nM (IC₅₀)

GSK-3β

260 nM (IC₅₀)

体外研究
(In Vitro)

R547 effectively inhibits CDK1/cyclin B, CDK2/cyclin E, and CDK4/cyclin D1 (Ki = 1–3 nmol/L) and is inactive (Ki > 5,000 nmol/L) against a panel of >120 unrelated kinases in cell-free assays^[4].
R547 effectively inhibits the proliferation of tumor cell lines independent of multidrug resistant status, histologic type, retinoblastoma protein, or p53 status, with IC₅₀s <0.60 μM^[4].
R547 reduces phosphorylation of the cellular retinoblastoma protein at specific CDK phosphorylation sites at the same concentrations that induced cell cycle arrest^[4].
R547 has anti-proliferative activity in tumor cells independent of p53, retinoblastoma, or MDR status^[4].
R547 blocks tumor cells in G1 plus G2 and induces apoptosis^[4].
R547 induces apoptosis as measured by DNA fragmentation^[4].
R547 inhibits phosphorylation of retinoblastoma protein in humantumor cells^[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay^[4]

Cell Line:	Human tumor cell lines (MDA-MB-468, MDA-MB-435, MCF-7, HCT116, SW480, RKO, HT-29, HCT15, H460a, C33A, DU145, OSA-CL, LOX, JEKO-1, REC-1)
Concentration:	MTT assay
Incubation Time:	5 days
Result:	Has potent in vitro antiproliferative activity.

Cell Cycle Analysis^[4]

Cell Line:	R547, HCT116
Concentration:	0.1 μM, 0.2 μM, 0.6 μM
Incubation Time:	20 hours
Result:	Decrease in BrdUrd incorporation and in percentage S phase in a dose-dependent, indicative of a cell cycle block in G1-S plus G2-M.

Western Blot Analysis^[4]

Cell Line:	HCT116 cells
Concentration:	0.1 μM, 0.2 μM, 0.6 μM
Incubation Time:	24 hours, 48 hours, 72 hours
Result:	Showed a band corresponding to a p48/retinoblastoma fragment that becomes more intense at 48 and 72 hours.

体内研究
(In Vivo)

R547 has significant in vivo efficacy with daily oral and once weekly i.v. dosing^[4].
R547 inhibits phosphorylation of retinoblastoma protein in tumors^[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	13-14 weeks old female immunodeficient nude mice (23-25 g), with HCT116/H460a/MDA-MB-435/DU145/LOX/A549 cells xenograft^[4]
Dosage:	40 mg/kg
Administration:	Oral administration; daily; for 3-weeks
Result:	Showed antitumor activity in all of the models in this study.

分子量

441.45

Formula

C₁₈H₂₁F₂N₅O₄S

CAS 号

741713-40-6

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : ≥ 50 mg/mL (113.26 mM)

* “≥” means soluble, but saturation unknown.

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.2653 mL	11.3263 mL	22.6526 mL
5 mM	0.4531 mL	2.2653 mL	4.5305 mL
10 mM	0.2265 mL	1.1326 mL	2.2653 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.5 mg/mL (5.66 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.66 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.5 mg/mL (5.66 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.66 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Chu XJ, DePinto W, Bartkovitz D, So SS, Vu BT, Packman K, Lukacs C, Ding Q, Jiang N, Wang K, Goelzer P, Yin X, Smith MA, Higgins BX, Chen Y, Xiang Q, Moliterni J, Kaplan G, Graves B, Lovey A, Fotouhi N.Discovery of [4-Amino-2-(1-methanesulfonylpiperidin-4-ylamino)pyrimidin-5-yl](2,3-difluoro-6- methoxyphenyl)methanone (R547), a potent and selective cyclin-dependent kinase inhibitor with significant in vivo antitumor activity.J Med Chem. 2006 Nov 2;49(22):6549-60.

[2]. Bayés M, Rabasseda X, Prous JR.Gateways to clinical trials. Methods Find Exp Clin Pharmacol. 2007 Jul-Aug;29(6):427-37.

[3]. Martin F, Thomson TM, Sewer A, Drubin DA, Mathis C, Weisensee D, Pratt D, Hoeng J, Peitsch MC.Assessment of network perturbation amplitudes by applying high-throughput data to causal biological networks.BMC Syst Biol. 2012 May 31;6:54.

[4]. DePinto, Wanda et al In vitro and in vivo activity of R547: a potent and selective cyclin-dependent kinase inhibitor currently in phase I clinical trials Molecular Cancer Therapeutics (2006), 5(11), 2644-2658

[5]. Jones, Clifford D.; Andrews, David M. Imidazole pyrimidine amides as potent, orally bioavailable cyclin-dependent kinase inhibitors Bioorganic & Medicinal Chemistry Letters (2008), 18(24), 6486-6489

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GDC-0152

发表于2025年12月19日由上海金畔生物科技有限公司

GDC-0152 纯度: 99.89%

GDC-0152 是一种有效的 IAPs 抑制剂，可以与 XIAP，cIAP1 和 cIAP2 的 BIR3 结合域，以及 ML-IAP 的 BIR 结合域结合，K_i 值分别为 28 nM，17 nM，43 nM 和 14 nM。

GDC-0152 Chemical Structure

CAS No. : 873652-48-3

规格	价格	是否有货
Free Sample (0.1-0.5 mg)		Apply now
10 mM * 1 mL in DMSO	￥820	In-stock
10 mg	￥1500	In-stock
50 mg	￥4500	In-stock
100 mg	￥7500	In-stock
200 mg		询价
500 mg		询价

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GDC-0152 相关产品

•相关化合物库:

Clinical Compound Library Plus
Bioactive Compound Library Plus
Apoptosis Compound Library
Anti-Cancer Compound Library
Clinical Compound Library
Anti-Breast Cancer Compound Library

生物活性

GDC-0152 is a potent IAPs inhibitor, and binds to the BIR3 domains of XIAP, cIAP1, cIAP2 and the BIR domain of ML-IAP with K_i values of 28 nM, 17 nM, 43 nM and 14 nM, respectively.

IC₅₀ & Target

Ki: 28 nM (XIAP BIR3), 14 nM (MLIAP-BIR3), 17 nM (cIAP1-BIR3), 43 nM (cIAP2-BIR3)

体外研究
(In Vitro)

GDC-0152 can block protein−protein interactions that involve IAP proteins and pro-apoptotic molecules. Using transiently transfected HEK293T cells, GDC-0152 is shown to disrupt XIAP binding to partially processed caspase-9 and to disrupt the association of ML-IAP, cIAP1, and cIAP2 with Smac. In melanoma SK-MEL28 cells, the endogenous association of ML-IAP and Smac is also effectively abolished by GDC-0152. GDC-0152 leads to a decrease in cell viability in the MDA-MB-231 breast cancer cell line, while having no effect on normal human mammary epithelial cells (HMEC). GDC-0152 is found to activate caspases 3 and 7 in a dose- and time-dependent manner. GDC-0152 is shown to induce rapid degradation of cIAP1 in A2058 melanoma cells. It effectively induces degradation of cIAP1 at concentrations as low as 10 nM, consistent with its affinity for cIAP1^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

GDC-0152 has moderate predicted hepatic clearance based on metabolic stability assays conducted using human liver microsomes. Plasma−protein binding of GDC-0152 is moderate and comparable among mice (88−91%), rats (89−91%), dogs (81−90%), monkeys (76−85%), and humans (75−83%) over the range of concentrations investigated (0.1−100 μM); higher plasma−protein binding is observed in rabbits (95−96%). GDC-0152 does not preferentially distribute to red blood cells with blood−plasma partition ratios ranging from 0.6 to 1.1 in all species tested. The pharmacokinetics for GDC-0152 is achieved with a C max of 53.7 μM and AUC of 203.5 h·μM^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial

分子量

498.64

Formula

C₂₅H₃₄N₆O₃S

CAS 号

873652-48-3

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : ≥ 100 mg/mL (200.55 mM)

Ethanol : 50 mg/mL (100.27 mM; Need ultrasonic)

* “≥” means soluble, but saturation unknown.

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.0055 mL	10.0273 mL	20.0545 mL
5 mM	0.4011 mL	2.0055 mL	4.0109 mL
10 mM	0.2005 mL	1.0027 mL	2.0055 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.5 mg/mL (5.01 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.01 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.5 mg/mL (5.01 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.01 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
3.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.5 mg/mL (5.01 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.01 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Flygare JA, et al. Discovery of a potent small-molecule antagonist of inhibitor of apoptosis (IAP) proteins and clinical candidate for the treatment of cancer (GDC-0152). J Med Chem. 2012 May 10;55(9):4101-13.

Kinase Assay ^[1]	Inhibition constants (K_i) for the antagonists are determined by addition of the IAP protein constructs to wells containing serial dilutions of the antagonists or the peptide AVPW, and the Hid-FAM probe or AVP-diPhe-FAM probe, as appropriate, in the polarization buffer. Samples are read after a 30-minute incubation. Fluorescence polarization values are plotted as a function of the antagonist concentration, and the IC₅₀ values are obtained by fitting the data to a 4-parameter equation using software. K_i values for the antagonists are determined from the IC₅₀ valued. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay ^[1]	Detached cells are washed with phosphate-buffered saline (PBS) and are resuspended in assay media (MDA-MB-231 cells: RPMI1640 supplemented with 10% fetal bovine serum and 2 mM L-glutamine [GlutaMAX-1]) or culture media (HMECs: MEBM^® with MEGM SingleQuots^®). Cells are placed in tissue culture-treated, white-wall or black-wall, clear-bottom, 96-well plates at 1×10⁴ cells/well in a volume of 50 μL. The plates are incubated at 37°C and 5% CO₂ overnight, the media is removed, and GDC-0152 or it’s enantiomer are added in assay media. Cells cultured in white-wall, clear-bottom plates are incubated at 37°C and 5% CO₂ for 3 days before cell viability is measured using the CellTiter-Glo^® luminescent cell viability assay kit. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration ^[1]	Cells are resuspended in PBS and the cell suspension is mixed 1:1 with Matrigel. The cells (1.5×10⁷) are then implanted subcutaneously into the right flank of 130 female nude mice aged 6-8 weeks. Tumor volumes are calculated. Ten mice with the appropriate mean tumor volume are assigned randomLy to each of six groups. The mean tumor volume±the standard error of the mean (SEM) for all six groups is 168±3 mm³ at the initiation of treatment (Day 0). Mice are dosed 1 or vehicle (PBS) by oral gavage with a dose volume of 4.0 mL/kg. The mice are observed on each day of the study, and tumor volumes and body weights are measured twice each week. Percent tumor growth inhibition is calculated using the formula %TGI=100× (1- Tumor Volumedose/Tumor Volumevehicle). 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献	[1]. Flygare JA, et al. Discovery of a potent small-molecule antagonist of inhibitor of apoptosis (IAP) proteins and clinical candidate for the treatment of cancer (GDC-0152). J Med Chem. 2012 May 10;55(9):4101-13.

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BAY-299

发表于2025年12月18日由上海金畔生物科技有限公司

BAY-299 纯度: 99.24%

BAY-299 是一种非常有效的双重抑制剂，抑制 BRPF2 溴结构域 (BD)，TAF1 BD2，和 TAF1L BD2，IC₅₀ 分别为 67 nM，8 nM 和 106 nM。

BAY-299 Chemical Structure

CAS No. : 2080306-23-4

规格	价格	是否有货
10 mM * 1 mL in DMSO	￥825	In-stock
5 mg	￥750	In-stock
10 mg	￥1250	In-stock
25 mg	￥2600	In-stock
50 mg	￥4200	In-stock
100 mg	￥7100	In-stock
200 mg		询价
500 mg		询价

* Please select Quantity before adding items.

BAY-299 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Epigenetics Compound Library
Histone Modification Research Compound Library
Anti-Cancer Compound Library
Reprogramming Compound Library
Chemical Probe Library
Anti-Blood Cancer Compound Library
Targeted Diversity Library

生物活性

BAY-299 is a very potent, dual inhibitor with IC₅₀s of 67 nM for BRPF2 bromodomains (BD), 8 nM for TAF1 BD2, and 106 nM for TAF1L BD2.

IC₅₀ & Target^[1]

BRPF2 BD

67 nM (IC₅₀)

BRPF1 BD

3150 nM (IC₅₀)

BRPF3 BD

5550 nM (IC₅₀)

TAF1 BD2

8 nM (IC₅₀)

TAF1L BD2

106 nM (IC₅₀)

体外研究
(In Vitro)

BAY-299 is a dual inhibitor of the bromodomain and PHD finger (BRPF) family member BRPF2 and the TATA box binding protein-associated factors TAF1 and TAF1L. TR-FRET assays showed that BAY-299 is a potent inhibitor of BRPF2 BD with an IC₅₀ of 67 nM, and a selectivity of 47- and 83-fold over BRPF1 and BRPF3 BDs. The profile of BAY-299 is further confirmed by AlphaScreen assay, where an IC₅₀ of 97 nM and a selectivity of 23- and 25-fold over BRPF1 and BRPF3 BDs are measured. NanoBRET experiments show that the interaction of BRPF2 BD with histones H4 and H3.3 is blocked by BAY-299 with IC₅₀ values of 575 and 825 nM, respectively. For TAF1 BD2, the IC₅₀ values are 970 and 1400 nM, respectively. No inhibitory effect is observed for the interaction between BRPF1 or BRD4 and histone H4 up to 10 μM for BAY-299. BAY-299 inhibits MOLM-13, MV4-11, 769-P, Jurkat, NCI-H526, CHL-1, and 5637 cells proliferation with GI₅₀s of 1060, 2630, 3210, 3900, 6860, 7400, and 7980 nM, respectively^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(In Vivo)

Studies of the in vivo pharmacokinetic properties of BAY-299 in rat reveal that blood clearance is low (ca. 17% of hepatic blood flow), volume of distribution in steady-state high, terminal half-life long to very long (t_1/2=10 h), and bioavailability high (F=73%). In vivo blood clearance is as anticipated based on rat liver microsome values but lower than expected based on hepatocyte data^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

429.47

Formula

C₂₅H₂₃N₃O₄

CAS 号

2080306-23-4

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : 25 mg/mL (58.21 mM; Need ultrasonic and warming)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.3285 mL	11.6423 mL	23.2845 mL
5 mM	0.4657 mL	2.3285 mL	4.6569 mL
10 mM	0.2328 mL	1.1642 mL	2.3285 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.5 mg/mL (5.82 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.82 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.5 mg/mL (5.82 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.82 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Bouché L, et al. Benzoisoquinolinediones as Potent and Selective Inhibitors of BRPF2 and TAF1/TAF1L Bromodomains. J Med Chem. 2017 May 11;60(9):4002-4022.

Cell Assay ^[1]	MOLM-13, MV4-11, 769-P, Jurkat, NCI-H526, CHL-1, and 5637 cell lines are treated with BAY-299 while in the logarithmic growth phase, and their viability is determined by AlamarBlue staining^[1]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration ^[1]	Rats^[1] BAY-299 is administered to three male Wistar rats per arm, either intravenously or intragastrally formulated as solutions. BAY-299 is given as i.v. bolus, and blood samples are taken at 2 min, 8 min, 15 min, 30 min, 45 min, 1 h, 2 h, 4 h, 6 h, 8 h, and 24 h after dosing. For pharmacokinetics after intragastral administration, BAY-299 is given intragastrally to fasted rats and blood samples are taken at 5 min, 15 min, 30 min, 45 min, 1 h, 2 h, 4 h, 6 h, 8 h, and 24 h after dosing. Blood is collected into lithium-heparin tubes and centrifuged for 15 min at 3000 rpm^[1]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献	[1]. Bouché L, et al. Benzoisoquinolinediones as Potent and Selective Inhibitors of BRPF2 and TAF1/TAF1L Bromodomains. J Med Chem. 2017 May 11;60(9):4002-4022.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

MS98

发表于2025年12月17日由上海金畔生物科技有限公司

MS98

MS98 是一种有效的选择性 PROTAC AKT 降解剂。MS98 消耗细胞总 AKT (T-AKT)，DC₅₀ 值为 78 nM。MS170 与 AKT1、AKT2 和 AKT3 结合，K_d 分别为 4 nM，140 nM 和 8.1 nM。

MS98 Chemical Structure

CAS No. : 2376137-31-2

规格		是否有货
100 mg		询价
250 mg		询价
500 mg		询价

* Please select Quantity before adding items.

生物活性

MS98 is a potent and selective PROTAC AKT degrader. MS98 depletes cellular total AKT (T-AKT) with the DC₅₀ value of 78 nM. MS98 binds to AKT1, AKT2, and AKT3 with K_ds of 4 nM, 140 nM, and 8.1 nM, respectively^[1].

IC₅₀ & Target

Akt1

4 nM ()

Akt2

140 nM ()

Akt3

8.1 nM ()

VHL

体外研究
(In Vitro)

The von Hippel-Lindau (VHL)-recruiting degrader MS98 is an effective AKT degrader. MS98 selectively induces robust AKT protein degradation, inhibits downstream signaling, and suppresses cancer cell proliferation. MS98 concentration- and time-dependently induces AKT degradation through the ubiquitin-proteasome system (UPS)^[1].
MS98 (10 nM-10 μM) effectively inhibits the proliferation in multiple cancer cell lines^[1].
MS98 (1 nM-10 μM) concentration-dependently depletes cellular total AKT (T-AKT) with the DC₅₀ value of 78±64 nM^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:	BT474, PC3, and MDA-MB-468 cells
Concentration:	10 nM, 100 nM, 1 μM, 10 μM
Incubation Time:	5 days
Result:	Inhibited the cell growth with GI₅₀s of 1.3±0.3 μM, 9.2±1.3 μM, and 3.8±1.2 μM for BT474 cells, PC3 cells, and MDA-MB-468 cells, respectively.

Western Blot Analysis^[1]

Cell Line:	BT474 cells
Concentration:	1 nM, 3 nM, 10 nM, 30 nM, 100 nM, 300 nM, 1 μM , 3 μM, and 10 μM
Incubation Time:	24 hours
Result:	Potently induced AKT degradation.

体内研究
(In Vivo)

MS98 (a single intraperitoneal injection at a dose of 50 mg/kg) is bioavailable in mice via IP injection. The maximum plasma concentration (C_max) reaches approximately 3.5 μM at 2 h, and the plasma concentrations remains above 3 μM over 8 h^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Male Swiss albino mice^[1]
Dosage:	Single 50 mg/kg(Pharmacokinetic Analysis)
Administration:	IP injection over 8 h
Result:	Bioavailable in mouse PK studies. The C_max is 3.5 μM at 2 h.

分子量

1097.84

Formula

C₅₈H₈₁ClN₁₀O₇S

CAS 号

2376137-31-2

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Yu X, et al. Design, Synthesis, and Evaluation of Potent, Selective, and Bioavailable AKT Kinase Degraders. J Med Chem. 2021;64(24):18054-18081.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

MS170

发表于2025年12月17日由上海金畔生物科技有限公司

MS170

MS170 是一种有效的选择性 PROTAC AKT 降解剂。MS170 消耗细胞总 AKT (T-AKT)，DC₅₀ 值为 32 nM。MS170 与 AKT1、AKT2 和 AKT3 结合，K_d 分别为 1.3 nM、77 nM 和 6.5 nM。

MS170 Chemical Structure

CAS No. : 2376136-61-5

规格		是否有货
5 mg		询价
10 mg		询价
50 mg		询价
100 mg		询价

* Please select Quantity before adding items.

生物活性

MS170 is a potent and selective PROTAC AKT degrader. MS170 depletes cellular total AKT (T-AKT) with the DC₅₀ value of 32 nM. MS170 binds to AKT1, AKT2, and AKT3 with K_ds of 1.3 nM, 77 nM, and 6.5 nM, respectively^[1].

IC₅₀ & Target

Akt1

1.3 nM (Kd)

Akt2

77 nM (Kd)

Akt3

6.5 nM (Kd)

CRBN-DDB1

体外研究
(In Vitro)

Cereblon (CRBN)-recruiting degrader MS170 is an effective AKT degrader without a ″hook effect″. MS170 selectively induces robust AKT protein degradation, inhibits downstream signaling, and suppresses cancer cell proliferation. MS170 concentration- and time-dependently induces AKT degradation through the ubiquitin-proteasome system (UPS)^[1].
MS170 (10 nM-10 μM) effectively inhibits the proliferation in multiple cancer cell lines^[1].
MS170 (1 nM-10 μM) concentration-dependently depletes cellular total AKT (T-AKT) with the DC₅₀ value of 32±18 nM^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[1]

Cell Line:	BT474, PC3, and MDA-MB-468 cells
Concentration:	10 nM, 100 nM, 1 μM, 10 μM
Incubation Time:	5 days
Result:	Inhibited the cell growth with GI₅₀s of 0.7±0.2 μM, 7.4±2.2 μM, and 5.7±2.4 μM for BT474 cells, PC3 cells, and MDA-MB-468 cells, respectively.

Western Blot Analysis^[1]

Cell Line:	BT474 cells
Concentration:	1 nM, 3 nM, 10 nM, 30 nM, 100 nM, 300 nM, 1 μM , 3 μM, and 10 μM
Incubation Time:	24 hours
Result:	Potently induced AKT degradation.

体内研究
(In Vivo)

MS170 (a single intraperitoneal injection at a dose of 50 mg/kg) is bioavailable in mice via IP injection^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Male Swiss albino mice^[1]
Dosage:	Single 50 mg/kg(Pharmacokinetic Analysis)
Administration:	IP injection over 8 h
Result:	Bioavailable in mouse PK studies. The C_max is1.4 μM at 2 h.

分子量

870.44

Formula

C₄₅H₅₆ClN₉O₇

CAS 号

2376136-61-5

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

参考文献

[1]. Yu X, et al. Design, Synthesis, and Evaluation of Potent, Selective, and Bioavailable AKT Kinase Degraders. J Med Chem. 2021;64(24):18054-18081.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

KDM5A-IN-1

发表于2025年12月16日由上海金畔生物科技有限公司

KDM5A-IN-1 纯度: 95.71%

KDM5A-IN-1 是一种有效的，口服可生物利用的泛组氨酸赖氨酸脱甲基酶 5 KDM5 抑制剂，对 KDM5A，KDM5B 和 KDM5C 的 IC₅₀ 值分别为 45 nM，56 nM 和 55 nM，对 PC9 H3K4Me3 的 EC₅₀ 值为 960 nM。KDM5A-IN-1 对其他 KDM 酶 (1A，2B，3B，4C，6A，7B) 的效力明显较低。

KDM5A-IN-1 Chemical Structure

CAS No. : 1905481-36-8

规格	价格	是否有货
10 mM * 1 mL in DMSO	￥4791	In-stock
1 mg	￥1500	In-stock
5 mg	￥3500	In-stock
10 mg	￥5000	In-stock
50 mg	￥15000	In-stock
100 mg	￥21000	In-stock
200 mg		询价
500 mg		询价

* Please select Quantity before adding items.

KDM5A-IN-1 相关产品

•相关化合物库:

Bioactive Compound Library Plus

生物活性

KDM5A-IN-1 is a potent, orally bioavailable pan-histone lysine demethylases 5 (KDM5) inhibitor with IC₅₀s of 45 nM, 56 nM and 55 nM for KDM5A, KDM5B and KDM5C, respectively, and with an EC₅₀ value of 960 nM for PC9 H3K4Me3. KDM5A-IN-1 is significantly less potent against other KDM5B enzymes (1A, 2B, 3B, 4C, 6A, 7B)^[1].

IC₅₀ & Target

IC50: 45 nM (KDM5A), 56 nM (KDM5B) and 55 nM (KDM5C)^[1]

体内研究
(In Vivo)

KDM5A-IN-1 (Compound 50, 5 mg/kg; oral administration; female CD-1 mice) treatment shows moderate clearance (28 mL/min/kg) in mice with good oral bioavailability (F% 34) and remarkably low plasma protein binding in mice (40%), with t_1/2 of 0.4 hours^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Female CD-1 mice^[1]
Dosage:	5 mg/kg
Administration:	Oral administration (Pharmacokinetic study)
Result:	Moderate clearance (28 mL/min/kg) in mice with good oral bioavailability (F% 34), and showed remarkably low plasma protein binding in mice (40%).

分子量

290.36

Formula

C₁₅H₂₂N₄O₂

CAS 号

1905481-36-8

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : ≥ 50 mg/mL (172.20 mM)

* “≥” means soluble, but saturation unknown.

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	3.4440 mL	17.2200 mL	34.4400 mL
5 mM	0.6888 mL	3.4440 mL	6.8880 mL
10 mM	0.3444 mL	1.7220 mL	3.4440 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.75 mg/mL (9.47 mM); Clear solution

此方案可获得 ≥ 2.75 mg/mL (9.47 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 27.5 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.75 mg/mL (9.47 mM); Clear solution

此方案可获得 ≥ 2.75 mg/mL (9.47 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 27.5 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
3.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.75 mg/mL (9.47 mM); Clear solution

此方案可获得 ≥ 2.75 mg/mL (9.47 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 27.5 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Liang J, et al. From a novel HTS hit to potent, selective, and orally bioavailable KDM5 inhibitors. Bioorg Med Chem Lett. 2017 Jul 1;27(13):2974-2981.

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BMS-3

发表于2025年12月15日由上海金畔生物科技有限公司

BMS-3 纯度: 99.46%

BMS-3 是一种高效的 LIMK 抑制剂，抑制 LIMK1 和 LIMK2，IC₅₀ 分别为 5 nM 和 6 nM。

BMS-3 Chemical Structure

CAS No. : 1338247-30-5

规格	价格	是否有货
10 mM * 1 mL in DMSO	￥990	In-stock
5 mg	￥900	In-stock
10 mg	￥1400	In-stock
50 mg	￥4200	In-stock
100 mg	￥7200	In-stock
200 mg		询价
500 mg		询价

* Please select Quantity before adding items.

BMS-3 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Cell Cycle/DNA Damage Compound Library
Kinase Inhibitor Library
Anti-Cancer Compound Library
Anti-Aging Compound Library
Anti-Lung Cancer Compound Library
Targeted Diversity Library

生物活性

BMS-3 is a potent LIMK inhibitor with IC₅₀s of 5 nM and 6 nM for LIMK1 and LIMK2, respectively.

IC₅₀ & Target^[1]

LIMK1

5 nM (IC₅₀)

LIMK2

6 nM (IC₅₀)

体外研究
(In Vitro)

BMS-3 (Compound 2) causes a dose-dependent reduction in cell count and induces mitotic arrest by increases in total nuclear DNA intensity and histone H3 phosphorylation after 24 h treatment in A549 human lung cancer cells. BMS-3 inhibits A549 human lung cancer cells with EC₅₀ value of 154 nM^[1]. BMS-3 is used to demonstrate the direct participation of LIMK1 in the phosphorylation of Cofilin. Inhibition of p-LIMK with 1-50 μM of BMS-3 results in a dose-dependent decrease of p-Cofilin after 10 min incubation in capacitating conditions. As a control, sperm are also incubated for 10 min under non-capacitating conditions which result in low levels of p-Cofilin. In the presence of 1 or 50 μM of BMS-3, actin polymerization levels are significantly lower compared to controls (DMSO). Mouse sperm are incubated under capacitating conditions for 90 min in the presence or absence of increasing concentrations of p-LIMK inhibitor BMS-3 (0, 1, 10 and 50 μM). The increasing concentrations of BMS-3 result in a strong decrease on the percentage of sperm that undergoes acrosomal exocytosis after stimulation with 20 μM of Progesterone^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

429.27

Formula

C₁₇H₁₂Cl₂F₂N₄OS

CAS 号

1338247-30-5

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : ≥ 100 mg/mL (232.95 mM)

* “≥” means soluble, but saturation unknown.

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.3295 mL	11.6477 mL	23.2954 mL
5 mM	0.4659 mL	2.3295 mL	4.6591 mL
10 mM	0.2330 mL	1.1648 mL	2.3295 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline

Solubility: ≥ 2.5 mg/mL (5.82 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.82 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.5 mg/mL (5.82 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.82 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
3.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.5 mg/mL (5.82 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.82 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Ross-Macdonald P, et al. Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors. Mol Cancer Ther. 2008 Nov;7(11):3490-8.

[2]. Romarowski A, et al. PKA-dependent phosphorylation of LIMK1 and Cofilin is essential for mouse sperm acrosomal exocytosis. Dev Biol. 2015 Sep 15;405(2):237-49.

Kinase Assay
^[1]

The protein kinase domains of human LIMK1 and LIMK2 are expressed as glutathione S-transferase fusion proteins using the Bac-to-Bac system in Sf9 cells. Compounds 1 to 6 (e.g., BMS-3) are assayed for inhibition of LIMK1 and LIMK2 protein kinase activity by radioactive phosphate incorporation into biotinylated full-length human destrin. Reactions are done with a concentration series of compound in 25 mM HEPES, 100 mM NaCl, 5 mM MgCl₂, 5 mM MnCl₂, 1 μM total ATP, 83 μg/mL biotinylated destrin, 167 ng/mL glutathione S-transferase-LIMK1, or 835 ng/mL glutathione S-transferase-LIMK2 in a total volume of 60 μL at room temperature for 30 min (LIMK1) or 60 min (LIMK2). Reactions are terminated by addition of 140 μL of 20% TCA/100 mM sodium pyrophosphate, and the precipitates are harvested onto GF/C unifilter plates. The radioactivity incorporated is determined using a TopCount after addition of 35 μL Microscint scintillation fluid^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

参考文献

[1]. Ross-Macdonald P, et al. Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors. Mol Cancer Ther. 2008 Nov;7(11):3490-8.

[2]. Romarowski A, et al. PKA-dependent phosphorylation of LIMK1 and Cofilin is essential for mouse sperm acrosomal exocytosis. Dev Biol. 2015 Sep 15;405(2):237-49.

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WZ4003

发表于2025年12月14日由上海金畔生物科技有限公司

WZ4003 纯度: 98.88%

WZ4003 是一种有效的，高度特异性的 NUAK kinase 抑制剂，能够抑制 NUAK1 (ARK5)/NUAK2 的活性，IC₅₀ 值分别为 20 nM/100 nM。

WZ4003 Chemical Structure

CAS No. : 1214265-58-3

规格	价格	是否有货
Free Sample (0.1-0.5 mg)		Apply now
10 mM * 1 mL in DMSO	￥1045	In-stock
5 mg	￥950	In-stock
10 mg	￥1450	In-stock
50 mg	￥3600	In-stock
100 mg		询价
200 mg		询价

* Please select Quantity before adding items.

WZ4003 相关产品

•相关化合物库:

Bioactive Compound Library Plus
Epigenetics Compound Library
Kinase Inhibitor Library
PI3K/Akt/mTOR Compound Library
Anti-Cancer Compound Library
Anti-Aging Compound Library
Antioxidants Compound Library
Oxygen Sensing Compound Library
Glycolysis Compound Library
Cytoskeleton Compound Library
Chemical Probe Library
Anti-Pancreatic Cancer Compound Library
Anti-Cancer Metabolism Compound Library
Lipid Metabolism Compound Library
Glucose Metabolism Compound Library
Targeted Diversity Library

生物活性

WZ4003 is the first potent and highly specific NUAK kinase inhibitor with IC₅₀ of 20 nM/100 nM for NUAK1 (ARK5)/NUAK2, without significant inhibition on other 139 kinases.

IC₅₀ & Target^[1]

NUAK1

20 nM (IC₅₀)

NUAK2

100 nM (IC₅₀)

体外研究
(In Vitro)

WZ4003 (3-10 μM) markedly suppresses NUAK1-mediated MYPT1 phosphorylation, in HEK-293 cells expressing wild-type NUAK1. Moreover, WZ4003 (10 μM) inhibits MYPT1 Ser445 phosphorylation as well as cell migration, invasion and proliferation to a similar extent as knock out in MEFs or knock down in U2OS cells of NUAK1^[1]. WZ4003 also exhibits a high, specific affinity to the L858R/T790M mutant EGFR, while a significantly reduced cellular IC₅₀ against T790M containing Ba/F3 cells^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

496.99

Formula

C₂₅H₂₉ClN₆O₃

CAS 号

1214265-58-3

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : 33.33 mg/mL (67.06 mM; Need ultrasonic)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.0121 mL	10.0606 mL	20.1211 mL
5 mM	0.4024 mL	2.0121 mL	4.0242 mL
10 mM	0.2012 mL	1.0061 mL	2.0121 mL

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

1.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.5 mg/mL (5.03 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.03 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
2.

请依序添加每种溶剂： 10% DMSO 90% corn oil

Solubility: ≥ 2.5 mg/mL (5.03 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (5.03 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在上海金畔生物科技有限公司网站选购。

参考文献

[1]. Banerjee S, et al. Characterization of WZ4003 and HTH-01-015 as selective inhibitors of the LKB1-tumour-suppressor-activated NUAK kinases. Biochem J. 2014 Jan 1;457(1):215-25.

[2]. Zhou W, et al. Novel mutant-selective EGFR kinase inhibitors against EGFR T790M. Nature. 2009 Dec 24;462(7276):1070-4

Kinase Assay ^[1]	In vitro activities of purified GST-NUAK1 and GST-NUAK1[A195T] are measured using Cerenkov counting of incorporation of radioactive ³²P from [γ-³²P]ATP into Sakamototide substrate peptide. Reactions are carried out in a 50 μL reaction volume for 30 min at 30°C and reactions are terminated by spotting 40 μL of the reaction mix on to P81 paper and immediately immersing in 50 mM orthophosphoric acid. Samples are washed three times in 50 mM orthophosphoric acid followed by a single acetone rinse and air drying. The kinase-mediated incorporation of [γ-³²P]ATP into Sakamototide is quantified by Cerenkov counting. One unit of activity is defined as that which catalysed the incorporation of 1 nmol of [³²P]phosphate into the substrate over 1 h. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay ^[1]	Cell proliferation assays are carried out colorimetrically in 96-well plates. Initially, 2000 cells per well are seeded for U2OS cells and 3000 cells per well are seeded for MEFs. The proliferation assays are carried out over 5 days in the presence or absence of 10 μM HTH-01-015 or WZ4003. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献	[1]. Banerjee S, et al. Characterization of WZ4003 and HTH-01-015 as selective inhibitors of the LKB1-tumour-suppressor-activated NUAK kinases. Biochem J. 2014 Jan 1;457(1):215-25. [2]. Zhou W, et al. Novel mutant-selective EGFR kinase inhibitors against EGFR T790M. Nature. 2009 Dec 24;462(7276):1070-4

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Envonalkib

发表于2025年12月13日由上海金畔生物科技有限公司

Envonalkib

Envonalkib 是一种有效和具有口服活性的 ALK 抑制剂，抑制 WT 和突变的 L1196M 和 G1269S-ALK 的 IC₅₀ 值分别为 1.96 nM，35.1 nM 和 61.3 nM。Envonalkib 可用于非小细胞肺癌的研究。

Envonalkib Chemical Structure

CAS No. : 1621519-26-3

规格		是否有货
100 mg		询价
250 mg		询价
500 mg		询价

* Please select Quantity before adding items.

生物活性	Envonalkib is a potent and orally active inhibitor of ALK, with IC₅₀s of 1.96 nM, 35.1 nM, and 61.3 nM for WT and mutated L1196M and G1269S-ALK. Envonalkib can be used for the research of non-small cell lung cancer^[1].
IC₅₀ & Target	IC50: 1.96 nM (WT-ALK), 35.1 nM (mutated L1196M-ALK), 61.3 nM (mutated G1269S-ALK)^[1]
体内研究 (In Vivo)	Envonalkib (formula I) (12.5-25 mg/kg; p.o. once daily for 14 days) inhibits the growth of human non-small cell lung cancer NCI-H2228 nude mice xenografts^[1]. Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量	506.40
Formula	C₂₄H₂₆Cl₂FN₅O₂
CAS 号	1621519-26-3
运输条件	Room temperature in continental US; may vary elsewhere.
储存方式	Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献	[1]. Feng G, et, al. Pyridine-substituted 2-aminopyridine protein kinase inhibitors. WO2016015676A1.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务