STAT3-IN-1 (compound 7d) is an excellent, selective and orally active STAT3 inhibitor, with IC50 values of 1.82 μM and 2.14 μM in HT29 and MDA-MB 231 cells, respectively. STAT3-IN-1 (compound 7d) induces tumor apoptosis[1].
IC50 & Target[1]
Stat-3
1.82 μM (IC50, in HT29 cells)
Stat-3
2.14 μM (IC50, in MDA-MB 231 cells)
体外研究 (In Vitro)
STAT3-IN-1 (compound 7d: 0-10 μM, 48 h) inhibits the STAT3 acetylation at lysine 685 and affected its specific genes expressions[1]. STAT3-IN-1 (compound 7d: 0-10 μM, 48 h) induces tumor cells apoptosis in MDA-MB-231 cells[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.
Apoptosis Analysis[1]
Cell Line:
MDA-MB-231 cell lines.
Concentration:
0-10 μM.
Incubation Time:
48 hours.
Result:
The induced apoptosis rates (early and late apoptosis) at 1, 2, 5, 8 and 10 μM were 9.0%, 11.2%, 20.9%, 43.3% and 85.2% versus control 3.0%.
Western Blot Analysis[1]
Cell Line:
MDA-MB-231 and HT-29 cell lines.
Concentration:
0-10 μM.
Incubation Time:
48 hours.
Result:
Inhibited STAT3 acetylation and STAT3 tyrosine phosphorylation in MDA-MB-231 cells. Increased the expressions of these tumor-suppressor genes (PTPN6 (SHP-1), CDKN2A and DLEC1) which were related to STAT3 acetylation at Lys685.
体内研究 (In Vivo)
STAT3-IN-1 (compound 7d: 10, 20 mg/kg, two weeks) arrests tumor growth with low toxicity in mouse-xenograft model[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:
Mouse-xenograft model bearing inoculation of mice breast cancer 4T1 cells[1].
Dosage:
10, 20 mg/kg.
Administration:
Oral administration once every other day for two weeks.
Result:
Arrested tumor growth with no obvious body weight loss.
分子量
475.53
Formula
C28H29NO6
CAS 号
2059952-75-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Li S, et al. Discovery of oral-available resveratrol-caffeic acid based hybrids inhibiting acetylated and phosphorylated STAT3 protein. Eur J Med Chem. 2016 Nov 29;124:1006-1018.
TPh A (Triphenyl Compound A) 是核蛋白 pirin 的有效抑制剂，其 Ki 值为0.6 uM。TPh A 破坏 Bcl3-pirin 复合物的形成。TPh A 可作为相关的小分子工具调控细胞内的 Pirin。
TPh A Chemical Structure
CAS No. : 21306-65-0
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生物活性
TPh A (Triphenyl Compound A) is a potent inhibitor of the nuclear protein pirin and binds specifically to pirin with a Ki of 0.6 uM. TPh A disrupts the formation of the bcl3–pirin complex. TPh A can be used as a novel small molecule tool to regulate pirin in cells[1].
体外研究 (In Vitro)
The Pirin is a nuclear protein with the nuclear factor I/CCAAT box transcription factor (NFI/CTF). Pirin proteins are highly conserved between mammals, plants, fungi, and prokaryotic organisms and are considered to belong to the cupin superfamily.TPh A (20 μM; 5 hours) reduces the amount of pirin-bound Bcl3 and inhibits the interaction between pirin and Bcl3 in HEK293T cells in a glutathione S-transferase (GST) pulldown assay (HEK293T cells are transfected with vectors that encoded bcl3-Myc and pirin-His6 for 43 h of transfection)[1].TPh A (0-100 μM; 48 hours) does not exert any potent cytotoxic activity against many human cancer cell lines, it against MCF7, MDA-MB231, HeLa, DU145, HepG2, A549, HT1080, WM266-4, and SK-MEL-28 cells with IC50 values >50 μM, and exhibits IC50 values of 27 μM, 20 μM and 26 μM for PC3 HL60 and HT29 cells, respectively[1].TPhA (0-50 μM; 48 hours) inhibits cell migration in WM266-4 cells, SK-MEL-28 cell in a concentration-dependent manner[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.
Glutaminase-IN-3 (compound 657) is a potent glutaminase inhibitor with an IC50 of 0.24 μM for Glutaminase 1 (GLS1). Glutaminase-IN-3 is extracted from patent WO2014089048A1, compound 657[1].
分子量
452.45
Formula
C19H19F3N6O2S
CAS 号
1439399-45-7
运输条件
Room temperature in continental US; may vary elsewhere.
Compound 401 is a synthetic inhibitor of DNA-PK (IC50 = 0.28 μM) that also targets mTOR but not PI3K in vitro.
IC50 & Target[1]
DNA-PK
0.28 μM (IC50)
mTOR
5.3 μM (IC50)
体外研究 (In Vitro)
Compound 401 is a potent inhibitor of DNA-PK (IC50=0.28 μM). Compound 401 is reported to be a poor inhibitor of PI3K, ATM, and ATR in vitro, but it is active against mTOR. Compound 401 shows activity against mTOR (IC50=5.3 μM) but not p110α/p85α PI3K (IC50>100 μM). Treatment of cells with Compound 401 blocks the phosphorylation of sites modified by mTOR-Raptor and mTOR-Rictor complexes (ribosomal protein S6 kinase 1 Thr389 and Akt Ser473, respectively). By contrast, there is no direct inhibition of Akt Thr308 phosphorylation, which is dependent on PI3K. Similar effects are also observed in cells that lack DNA-PK. Compound 401 inhibits immunoprecipitated epitope-tagged mTOR or endogenous mTOR in Raptor immunoprecipitates. In both cases, inhibition of 67% or 78% is obtained at 5 μM or 10 μM Compound 401, respectively. By contrast, dose response curves show that the p110α/p85α or p110β/p85α PI3K complexes are poorly inhibited by Compound 401 at these concentrations. The proliferation of TSC1-/- fibroblasts is inhibited in the presence of Compound 401, but TSC1+/+ cells are resistant[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
281.31
Formula
C16H15N3O2
CAS 号
168425-64-7
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 : 6 mg/mL (21.33 mM; Need ultrasonic and warming)
[1]. Ballou LM, et al. Inhibition of mammalian target of rapamycin signaling by 2-(morpholin-1-yl)pyrimido[2,1-alpha]isoquinolin-4-one. J Biol Chem. 2007 Aug 17;282(33):24463-70.
Kinase Assay [1]
FreeStyle 293-F cells are transfected with cDNA for AU1-mTOR using 293fectin. Two days later, the cells are lysed and mTOR immunoprecipitates are prepared using AU1 antibody. Alternatively, the mTORC1 complex is immunoprecipitated from untransfected cells using Raptor antibody. Kinase activity in the immunoprecipitates is assayed in the presence of vehicle (DMSO) or Compound 401 (1, 5 and 10 μM) using bacterially expressed glutathione S-transferase (GST)-4E-BP1 as a substrate. Kinase reactions are stopped by boiling in SDS sample buffer and the samples are subjected to SDS-PAGE. Phosphorylated 4E-BP1 is detected by autoradiography. Radioactivity in the bands is quantified by scintillation counting[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]. Ballou LM, et al. Inhibition of mammalian target of rapamycin signaling by 2-(morpholin-1-yl)pyrimido[2,1-alpha]isoquinolin-4-one. J Biol Chem. 2007 Aug 17;282(33):24463-70.
AKT-IN-3 (compound E22) is a potent, orally active low hERG blocking Akt inhibitor, with 1.4 nM, 1.2 nM and 1.7 nM for Akt1, Akt2 and Akt3, respectively. AKT-IN-3 (compound E22) also exhibits good inhibitory activity against other AGC family kinases, such as PKA, PKC, ROCK1, RSK1, P70S6K, and SGK. AKT-IN-3 (compound E22) induces apoptosis and inhibits metastasis of cancer cells[1].
IC50 & Target[1]
Akt1
1.4 nM (IC50)
Akt2
1.2 nM (IC50)
Akt3
1.7 nM (IC50)
PKA
0.3 nM (IC50)
P70S6K
8.9 (IC50)
分子量
526.36
Formula
C23H23Cl2F2N5O3
CAS 号
2374740-21-1
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]. Dong X, et al. Discovery of 3,4,6-Trisubstituted Piperidine Derivatives as Orally Active, Low hERG Blocking Akt Inhibitors via Conformational Restriction and Structure-Based Design. J Med Chem. 2019 Aug 8;62(15):7264-7288.
TH1338 (compound 3b), an orally active camptothecin derivative and a potent chemotherapeutic agent for cancer, demonstrates excellent cytotoxic potency against human tumor cell lines in vitro. TH1338 (compound 3b) possesses significant brain penetration, favorable efflux pump properties, and hematological toxicity profile[1][2].
体外研究 (In Vitro)
TH1338 (compound 3b) demonstrates significant brain penetration when dosed orally in mice[1]. TH1338 (compound 3b) exhibits potent anti-tumor activity in H460 (NSCLC) human tumor xenograft model[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:
H460 (NSCLC) human tumor xenograft model.
Concentration:
40 mg/kg.
Incubation Time:
Oral gavage.
Result:
Exhibited superior antitumor activity.
分子量
391.42
Formula
C22H21N3O4
CAS 号
1258494-60-8
运输条件
Room temperature in continental US; may vary elsewhere.
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]. Jian-Xin Duan, et al. 14-Aminocamptothecins: their synthesis, preclinical activity, and potential use for cancer treatment. J Med Chem. 2011 Mar 24;54(6):1715-23.
[2]. Xia Cheng, et al. Preparation, Characterization, and In Vivo Study of 7-Ethyl-14-Aminocamptothecin-Loaded Poly(Ethylene Glycol)2000 -Poly(Lactic Acid)2000 Polymeric Micelles Against H460 Human Nonsmall Cell Lung Carcinoma. J Pharm Sci. 2015 Nov;104(11):3934-3942.
TH1338 (compound 3b), an orally active camptothecin derivative and a potent chemotherapeutic agent for cancer, demonstrates excellent cytotoxic potency against human tumor cell lines in vitro. TH1338 (compound 3b) possesses significant brain penetration, favorable efflux pump properties, and hematological toxicity profile[1][2].
体外研究 (In Vitro)
TH1338 (compound 3b) demonstrates significant brain penetration when dosed orally in mice[1]. TH1338 (compound 3b) exhibits potent anti-tumor activity in H460 (NSCLC) human tumor xenograft model[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.
Cell Viability Assay[1]
Cell Line:
H460 (NSCLC) human tumor xenograft model.
Concentration:
40 mg/kg.
Incubation Time:
Oral gavage.
Result:
Exhibited superior antitumor activity.
分子量
391.42
Formula
C22H21N3O4
CAS 号
1258494-60-8
运输条件
Room temperature in continental US; may vary elsewhere.
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 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Jian-Xin Duan, et al. 14-Aminocamptothecins: their synthesis, preclinical activity, and potential use for cancer treatment. J Med Chem. 2011 Mar 24;54(6):1715-23.
[2]. Xia Cheng, et al. Preparation, Characterization, and In Vivo Study of 7-Ethyl-14-Aminocamptothecin-Loaded Poly(Ethylene Glycol)2000 -Poly(Lactic Acid)2000 Polymeric Micelles Against H460 Human Nonsmall Cell Lung Carcinoma. J Pharm Sci. 2015 Nov;104(11):3934-3942.
TH1338 (compound 3b), an orally active camptothecin derivative and a potent chemotherapeutic agent for cancer, demonstrates excellent cytotoxic potency against human tumor cell lines in vitro. TH1338 (compound 3b) possesses significant brain penetration, favorable efflux pump properties, and hematological toxicity profile[1][2].
体外研究 (In Vitro)
TH1338 (compound 3b) demonstrates significant brain penetration when dosed orally in mice[1]. TH1338 (compound 3b) exhibits potent anti-tumor activity in H460 (NSCLC) human tumor xenograft model[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:
H460 (NSCLC) human tumor xenograft model.
Concentration:
40 mg/kg.
Incubation Time:
Oral gavage.
Result:
Exhibited superior antitumor activity.
分子量
391.42
Formula
C22H21N3O4
CAS 号
1258494-60-8
运输条件
Room temperature in continental US; may vary elsewhere.
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]. Jian-Xin Duan, et al. 14-Aminocamptothecins: their synthesis, preclinical activity, and potential use for cancer treatment. J Med Chem. 2011 Mar 24;54(6):1715-23.
[2]. Xia Cheng, et al. Preparation, Characterization, and In Vivo Study of 7-Ethyl-14-Aminocamptothecin-Loaded Poly(Ethylene Glycol)2000 -Poly(Lactic Acid)2000 Polymeric Micelles Against H460 Human Nonsmall Cell Lung Carcinoma. J Pharm Sci. 2015 Nov;104(11):3934-3942.
NOD1/2 antagonist-1 (compound 36b) is a potent NOD1/2 (nucleotide-binding oligomerization domain-like receptor 1/2) dual antagonist, with IC50 values of 1.13 (NOD1) and 0.77 μM (NOD2), respectively. NOD1/2 antagonist-1 has a acceptable T1/2 (67.6 min). NOD1/2 antagonist-1 (compound 36b) can improve the antitumor efficacy of Paclitaxel (PTX)[1].
IC50 & Target
NOD1
1.13 μM (IC50)
NOD2
0.77 μM (IC50)
体外研究 (In Vitro)
NOD1/2 antagonist-1 (compound 36b) (0-10 μM, 3 h) inhibits C12-iE-DAP-induced or MDP-induced NF-κB activation[1]. NOD1/2 antagonist-1 (0-10 μM, 1 h) suppresses inflammation via NOD1 and NOD2 activation[1]. NOD1/2 antagonist-1 (0-10 μM, 1 h) consistently and dose-dependently reduces the transcription of IL-6, TNF-α and IL-8, respectively[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay
Cell Line:
HEK-Blue hNOD1 and HEK-Blue hNOD2 cells[1]
Concentration:
0.001, 0.01, 0.1, 1, 10 μM
Incubation Time:
3 h
Result:
Inhibited C12-iE-DAP-induced or MDP-induced NF-κB activation, and had no or little effect on cell growth.
Western Blot Analysis
Cell Line:
THP-1 cells[1]
Concentration:
1, 10 μM
Incubation Time:
1 h
Result:
Prevented the increases in p-RIP2, p-IKKα/β, p-p65, p-p38, and p-JNK and the degradation of IκBα in a dose-dependent manner, and blocked NOD1-and NOD2-mediated inflammatory cytokine secretion in THP-1 cells.
RT-PCR
Cell Line:
THP-1 cells[1]
Concentration:
1, 10 μM
Incubation Time:
1 h
Result:
Consistently and dose-dependently reduced the transcription of IL-6, TNF-α and IL-8 stimulated by C12-iE-DAP or MDP, respectively.
体内研究 (In Vivo)
NOD1/2 antagonist-1 (compound 36b) (50 mg/kg, IV, once every other day, for 16 days) improves the antitumor efficacy of PTX in B16 tumor-bearing model[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
C57BL/6 mice (6-8 weeks old, male, B16 tumor-bearing model, 4 groups, n = 7 each group)[1]
Dosage:
50 mg/kg (36b), 50 mg/kg (36b) + 12 mg/kg (PTX) (formulated in DMSO/Cremophor EL/saline at 5:5:90(v:v:v))
Administration:
IV, once every other day (36b), once every 4 days (PTX), for 16 days
Result:
Significantly reduced tumor growth compared with PTX treatment alone, and the tumor weight inhibitory rate increased from 64.07% to 85.46%.
分子量
663.03
Formula
C32H28ClF5N4O4
CAS 号
2704623-69-6
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]. Ma Y, Yang J, Wei X, et al. Nonpeptidic quinazolinone derivatives as dual nucleotide-binding oligomerization domain-like receptor 1/2 antagonists for adjuvant cancer chemotherapy. Eur J Med Chem. 2020;207:112723.
Dorsomorphin (Compound C) is a selective and ATP-competitive AMPK inhibitor (Ki=109 nM in the absence of AMP). Dorsomorphin (BML-275) selectively inhibits BMP type I receptors ALK2, ALK3, and ALK6. Dorsomorphin induces autophagy[1][2].
IC50 & Target[1][2]
AMPK
109 nM (Ki)
ALK2
ALK3
ALK6
Autophagy
体外研究 (In Vitro)
Dorsomorphin (compound C) (0-10 μM, 18 h) suppresses 2DG-induced GRP78 promoter activity in human fibrosarcoma HT1080 cells in a dose-dependent manner but has little effect on tunicamycin-induced GRP78 promoter activity. Dorsomorphin (compound C) C also suppresses GRP78 promoter activity induced by glucose withdrawal. Dorsomorphin (compound C) has no effect on 2DG-induced PERK activation and reduces the both basal and 2DG-induced AMPK phosphorylation levels in HT1080 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.
Western Blot Analysis[2]
Cell Line:
Human fibrosarcoma HT1080 cells
Concentration:
0-10 μM.
Incubation Time:
18 hours.
Result:
Suppressed 2DG-induced GRP78 promoter activity in a dose-dependent manner and also suppressed GRP78 promoter activity induced by glucose withdrawal.
体内研究 (In Vivo)
Dorsomorphin (compound C: 10 mg/kg, intravenously once) treatment leads to a 60% increase in total serum iron concentrations, reduces basal levels of hepcidin expression and increasing serum iron concentrations in adult mice[3]. Dorsomorphin (compound C: 0.2 mg/kg, I.V., 30 min before LPS injection) reduces ICAM-1 and VCAM-1 expression in LPS-injected rat aorta[4]. Dorsomorphin (compound C; 25 mg/kg; i.p. injection; in male BALB/c mice) treatment before lipopolysaccharide (LPS) injection significantly reduces lethality in contrast to animals treated with LPS challenge only[5].
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:
Wild-type (WT) C57BL/6 adult mice that are fed a standard iron-replete diet express high levels of hepcidin[3].
Dosage:
10 mg/kg.
Administration:
Intravenously once.
Result:
Led to a 60% increase in total serum iron concentrations. Effective in reducing basal levels of hepcidin expression and increasing serum iron concentrations in adult mice.
Animal Model:
Male Sprague-Dawley rats, 8 weeks of age (body weight 230-250 g)[4].
Dosage:
0.2 mg/kg.
Administration:
I.V., 30 min before LPS injection.
Result:
Reduced ICAM-1 and VCAM-1 expression in LPS-injected rat aorta.
Animal Model:
Male BALB/c mice at 6-7 weeks of age weighing 20-22 g[5]
Dosage:
25 mg/kg
Administration:
Injection i.p.; 60 min before LPS challenge
Result:
Treatment of mice with 25 mg/kg before LPS injection significantly reduced lethality in contrast to animals treated with LPS challenge only.
分子量
399.49
Formula
C24H25N5O
CAS 号
866405-64-3
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Zhou G, et al. Role of AMP-activated protein kinase in mechanism of action. J Clin Invest. 2001 Oct;108(8):1167-74.
[2]. Kim YM, et al. Compound C independent of AMPK inhibits ICAM-1 and VCAM-1 expression in inflammatory stimulants-activated endothelial cells in vitro and in vivo. Atherosclerosis. 2011 Nov;219(1):57-64.
[3]. Saito S, et al. Compound C prevents the unfolded protein response during glucose deprivation through a mechanism independent of AMPK and BMP signaling. PLoS One. 2012;7(9):e45845.
[4]. Guo Y, et al. AMPK inhibition blocks ROS-NFκB signaling and attenuates endotoxemia-induced liver injury. PLoS One. 2014 Jan 24;9(1):e86881.
[5]. Yu PB, et al. Dorsomorphin inhibits BMP signals required for embryogenesis and iron metabolism. Nat Chem Biol. 2008 Jan;4(1):33-41.
Dorsomorphin dihydrochloride(Synonyms: Compound C dihydrochloride; BML-275 dihydrochloride) 纯度: 99.73%
Dorsomorphin dihydrochloride (Compound C dihydrochloride) 是一种有效，选择性和 ATP 竞争性的 AMPK 抑制剂，Ki 为 109 nM。Dorsomorphin dihydrochloride 通过靶向抑制 I 型受体 ALK2，ALK3 和 ALK6 来抑制 BMP 途径。Dorsomorphin dihydrochloride 诱导自噬 (autophagy) 作用。
Dorsomorphin dihydrochloride Chemical Structure
CAS No. : 1219168-18-9
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是否有货
数量
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Apply now
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￥716
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5 mg
￥651
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10 mg
￥950
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50 mg
￥3464
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100 mg
￥5400
In-stock
200 mg
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500 mg
询价
* Please select Quantity before adding items.
Dorsomorphin dihydrochloride 相关产品
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Anti-Colorectal Cancer Compound Library
生物活性
Dorsomorphin dihydrochloride (BML-275 dihydrochloride; Compound C dihydrochloride) is a potent, selective and ATP-competitive AMPK inhibitor, with a Ki of 109 nM[1]. Dorsomorphin dihydrochloride inhibits BMP pathway by targeting the type I receptors ALK2, ALK3, and ALK6. Dorsomorphin dihydrochloride induces autophagy[2].
IC50 & Target[1][2]
AMPK
109 nM (Ki)
ALK2
ALK3
ALK6
Autophagy
体外研究 (In Vitro)
Dorsomorphin (compound C) (0-10 μM, 18 h) suppresses 2DG-induced GRP78 promoter activity in human fibrosarcoma HT1080 cells in a dose-dependent manner but has little effect on tunicamycin-induced GRP78 promoter activity. Dorsomorphin (compound C) C also suppresses GRP78 promoter activity induced by glucose withdrawal. Dorsomorphin (compound C) has no effect on 2DG-induced PERK activation and reduces the both basal and 2DG-induced AMPK phosphorylation levels in HT1080 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.
Western Blot Analysis[2]
Cell Line:
Human fibrosarcoma HT1080 cells.
Concentration:
0-10 μM.
Incubation Time:
18 hours
Result:
Suppressed 2DG-induced GRP78 promoter activity in a dose-dependent manner and also suppressed GRP78 promoter activity induced by glucose withdrawal.
体内研究 (In Vivo)
Dorsomorphin (compound C: 10 mg/kg, intravenously once) treatment leads to a 60% increase in total serum iron concentrations, reduces basal levels of hepcidin expression and increasing serum iron concentrations in adult mice[3]. Dorsomorphin (compound C: 0.2 mg/kg, i.v., 30 min before LPS injection) reduces ICAM-1 and VCAM-1 expression in LPS-injected rat aorta[4]. Dorsomorphin (compound C; 25 mg/kg; i.p. injection, in male BALB/c mice) treatment before lipopolysaccharide (LPS) injection significantly reduces lethality in contrast to animals treated with LPS challenge only[5].
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:
Wild-type (WT) C57BL/6 adult mice that are fed a standard iron-replete diet express high levels of hepcidin[3].
Dosage:
10 mg/kg.
Administration:
Intravenously once.
Result:
Led to a 60% increase in total serum iron concentrations. Effective in reducing basal levels of hepcidin expression and increasing serum iron concentrations in adult mice.
Animal Model:
Male Sprague-Dawley rats, 8 weeks of age (body weight 230-250 g)[4].
Dosage:
0.2 mg/kg.
Administration:
I.V., 30 min before LPS injection.
Result:
Reduced ICAM-1 and VCAM-1 expression in LPS-injected rat aorta.
Animal Model:
Male BALB/c mice at 6-7 weeks of age weighing 20-22 g[5]
Dosage:
25 mg/kg
Administration:
Injection i.p.; 60 min before LPS challenge
Result:
Treatment of mice with 25 mg/kg before LPS injection significantly reduced lethality in contrast to animals treated with LPS challenge only.
分子量
472.41
Formula
C24H27Cl2N5O
CAS 号
1219168-18-9
运输条件
Room temperature in continental US; may vary elsewhere.
Solubility: 65 mg/mL (137.59 mM); Clear solution; Need ultrasonic
*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]. Zhou G, et al. Role of AMP-activated protein kinase in mechanism of action. J Clin Invest. 2001 Oct;108(8):1167-74.
[2]. Saito S, et al. Compound C prevents the unfolded protein response during glucose deprivation through a mechanism independent of AMPK and BMP signaling. PLoS One. 2012;7(9):e45845.
[3]. Yu PB, et al. Dorsomorphin inhibits BMP signals required for embryogenesis and iron metabolism. Nat Chem Biol. 2008 Jan;4(1):33-41.
[4]. Kim YM, et al. Compound C independent of AMPK inhibits ICAM-1 and VCAM-1 expression in inflammatory stimulants-activated endothelial cells in vitro and in vivo. Atherosclerosis. 2011 Nov;219(1):57-64.
[5]. Guo Y, et al. AMPK inhibition blocks ROS-NFκB signaling and attenuates endotoxemia-induced liver injury. PLoS One. 2014 Jan 24;9(1):e86881.
Compound E 是 γ-secretase 抑制剂。 Compound E 抑制 β-amyloid(40)，β-amyloid(42)，和Notch γ-分泌酶切割的 IC50 值分别为 0.24，0.37，0.32 nM。
Compound E Chemical Structure
CAS No. : 209986-17-4
规格
价格
是否有货
数量
1 mg
￥1600
In-stock
5 mg
￥5200
In-stock
10 mg
￥9200
In-stock
25 mg
￥19000
In-stock
50 mg
询价
100 mg
询价
* Please select Quantity before adding items.
Compound E 相关产品
•相关化合物库:
Bioactive Compound Library Plus
生物活性
Compound E is a γ-secretase inhibitor. Compound E bloks β-amyloid(40), β-amyloid(42), and Notch γ-secretase cleavage with IC50s of 0.24, 0.37, 0.32 nM, respectively.
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 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Beher D, et al. Pharmacological knock-down of the presenilin 1 heterodimer by a novel gamma -secretase inhibitor: implications for presenilin biology. J Biol Chem. 2001 Nov 30;276(48):45394-402.
[2]. Rasul S, et al. Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells. Br J Cancer. 2009 Jun 16;100(12):1879-88.
Cell Assay [1]
The breast cancer cell lines MDA-MB-231, T47D, and MCF-7 are treated with Compound E at concentrations in the range 0.01-50 μM for 48 h and their viability is determined using a Coulter counter[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]. Beher D, et al. Pharmacological knock-down of the presenilin 1 heterodimer by a novel gamma -secretase inhibitor: implications for presenilin biology. J Biol Chem. 2001 Nov 30;276(48):45394-402.
[2]. Rasul S, et al. Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells. Br J Cancer. 2009 Jun 16;100(12):1879-88.
PI3K-IN-6 (compound 20a) is an oral active and highly selective phosphoinositide 3-kinase (PI3K) β/δ inhibitor, with IC50 values of 7.8 nM/5.3 nM for PI3K β/δ, respectively. PI3K-IN-6 (compound 20a) has potential top treat phosphatase and tensin homolog (PTEN) feficient tumors[1].
IC50 & Target
PI3Kβ
7.8 nM (IC50)
PI3Kδ
5.3 nM (IC50)
PI3Kα
850 nM (IC50)
分子量
450.26
Formula
C17H14Cl2FN9O
CAS 号
1842380-77-1
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]. Perreault S, et al. Discovery of a Phosphoinositide 3-Kinase (PI3K) β/δ Inhibitor for the Treatment of Phosphatase and Tensin Homolog (PTEN) Deficient Tumors: Building PI3Kβ Potency in a PI3Kδ-Selective Template by Targeting Nonconserved Asp856. J Med Chem. 2017 Feb 23;60(4):1555-1567.
Glutaminase C-IN-1 (Compound 968) 是 Glutaminase C 变构抑制剂。
Glutaminase C-IN-1 Chemical Structure
CAS No. : 311795-38-7
规格
价格
是否有货
数量
10 mM * 1 mL in DMSO
￥990
In-stock
5 mg
￥900
In-stock
10 mg
￥1300
In-stock
50 mg
￥5200
In-stock
100 mg
询价
200 mg
询价
* Please select Quantity before adding items.
Glutaminase C-IN-1 相关产品
•相关化合物库:
Bioactive Compound Library Plus
Metabolism/Protease Compound Library
Anti-Cancer Compound Library
Glutamine Metabolism Compound Library
Anti-Cancer Metabolism Compound Library
Mitochondria-Targeted Compound Library
Targeted Diversity Library
生物活性
Glutaminase C-IN-1 (Compound 968) is an allosteric inhibitor of Glutaminase C that inhibits cancer cell growth without affecting their normal cellular counterparts.
分子量
475.42
Formula
C27H27BrN2O
CAS 号
311795-38-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Stalnecker CA, et al. Mechanism by which a recently discovered allosteric inhibitor blocks glutamine metabolism in transformed cells. Proc Natl Acad Sci U S A. 2015 Jan 13;112(2):394-9.
CCR4 antagonist 2 (Compound 31) is a novel potent, orally bioavailable small molecule antagonists of CC chemokine receptor 4 (CCR4) that inhibits Treg trafficking into the Tumor Microenvironment without suppressing the number of Treg in healthy tissues. CCR4 antagonist 2 (Compound 31) exhibits IC50 values of Ca2+flux and (chemotaxis) CTX are 40 nM and 70 nM, respectively[1].
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]. Jackson JJ, et al. Discovery of a Potent and Selective CCR4 Antagonist That Inhibits Treg Trafficking into the Tumor Microenvironment. J Med Chem. 2019 Jul 11;62(13):6190-6213.
Cdc7-IN-5 (compound I-B) is a potent Cdc7 kinase inhibitor extracted from patent WO2019165473A1, compound I-B. Cdc7 is a serine-threonine protein kinase enzyme which is essential for the initiation of DNA replication in the cell cycle[1].
分子量
445.47
Formula
C25H23N3O5
CAS 号
1402057-86-6
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 : 12.5 mg/mL (28.06 mM; ultrasonic and warming and heat to 60°C)
Compound 48/80 (Poly-p-methoxyphenethylmethylamine) 作为选择性肥大细胞激活剂广泛用于动物和组织模型。Compound 48/80 作用于肥大细胞膜，刺激三聚体 G 蛋白，并通过磷脂酶 C 和 D 途径诱导脱颗粒。
Compound 48/80 Chemical Structure
CAS No. : 94724-12-6
规格
是否有货
100 mg
询价
250 mg
询价
500 mg
询价
* Please select Quantity before adding items.
Compound 48/80 的其他形式现货产品:
Compound 48/80 trihydrochloride
生物活性
Compound 48/80 (Poly-p-methoxyphenethylmethylamine) is widely used in animal and tissue models as a “selective” mast cell activator. Compound 48/80 acts at the mast cell membrane to stimulate trimeric G-proteins and induces degranulation via phospholipase C and D pathways[1][2].
IC50 & Target
Mast Cell Activator[1]
体外研究 (In Vitro)
Compound 48/80 (poly-p-methoxyphenethylmethylamine), an agent commonly used to trigger degranulation of mast cells, at concentrations of 5-20 μg/ml suppresses the proliferation of L1210 and Friend leukemic cells in vitro, inducing the formation of giant cells, which are polykaryons[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
519.72
Formula
C32H45N3O3
CAS 号
94724-12-6
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]. Schemann M, et al. The mast cell degranulator compound 48/80 directly activates neurons. PLoS One. 2012;7(12):e52104.
[2]. Wang YH, Taché Y, Harris AG, Kreutner W, Daly AF, Wei JY. Desloratadine prevents compound 48/80-induced mast cell degranulation: visualization using a vital fluorescent dye technique. Allergy. 2005;60(1):117-124.
[3]. Darzynkiewicz Z, Carter S. Compound 48/80 impairs cytokinesis in murine leukemic cells. J Cell Physiol. 1984;119(1):1-6.
