Siramesine (Lu 28-179) is a potent sigma-2 receptor agonist. Siramesine has a subnanomolar affinity for sigma-2 receptors (IC50=0.12 nM) and exhibits a 140-fold selectivity for sigma-2 receptors over sigma-1 receptors (IC50=17 nM). Siramesine triggers cell death through destabilisation of mitochondria, but not lysosomes. Anti-cancer activity[1][2][3].
体外研究 (In Vitro)
Siramesine displays the binding affinities: IC50 (sigma 1)=17 nM, IC50 (sigma 2)=0.12 nM, IC50 (5-HT1A)=21000 nM, IC50 (5-HT1A)=2000 nM, IC50 (D2)=800 nM, IC50 (alpha 1)=330 nM[1]. Siramesine (0-50μM; 8 hours) induces cell death in various cell lines (HaCaT, Hsc-4, HeLa and MCF-7, neuroblastoma cell line SH-SY5Y and glioblastoma cell line U-87MG)[2]. Siramesine (0-40 μM; 2-48 hours) activates caspases in HaCaT and in U-87MG cells[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
454.58
Formula
C30H31FN2O
CAS 号
147817-50-3
中文名称
西拉美新
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]. Perregaard J, et al. Sigma ligands with subnanomolar affinity and preference for the sigma 2 binding site. 1. 3-(omega-aminoalkyl)-1H-indoles. J Med Chem. 1995;38(11):1998-2008.
[2]. Česen MH, et al. Siramesine triggers cell death through destabilisation of mitochondria, but not lysosomes. Cell Death Dis. 2013;4(10):e818. Published 2013 Oct 3.
[3]. Ostenfeld MS, et al. Anti-cancer agent siramesine is a lysosomotropic detergent that induces cytoprotective autophagosome accumulation. Autophagy. 2008;4(4):487-499.
Siramesine (Lu 28-179) is a potent sigma-2 receptor agonist. Siramesine has a subnanomolar affinity for sigma-2 receptors (IC50=0.12 nM) and exhibits a 140-fold selectivity for sigma-2 receptors over sigma-1 receptors (IC50=17 nM). Siramesine triggers cell death through destabilisation of mitochondria, but not lysosomes. Anti-cancer activity[1][2][3].
体外研究 (In Vitro)
Siramesine displays the binding affinities: IC50 (sigma 1)=17 nM, IC50 (sigma 2)=0.12 nM, IC50 (5-HT1A)=21000 nM, IC50 (5-HT1A)=2000 nM, IC50 (D2)=800 nM, IC50 (alpha 1)=330 nM[1]. Siramesine (0-50μM; 8 hours) induces cell death in various cell lines (HaCaT, Hsc-4, HeLa and MCF-7, neuroblastoma cell line SH-SY5Y and glioblastoma cell line U-87MG)[2]. Siramesine (0-40 μM; 2-48 hours) activates caspases in HaCaT and in U-87MG 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
454.58
Formula
C30H31FN2O
CAS 号
147817-50-3
中文名称
西拉美新
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]. Perregaard J, et al. Sigma ligands with subnanomolar affinity and preference for the sigma 2 binding site. 1. 3-(omega-aminoalkyl)-1H-indoles. J Med Chem. 1995;38(11):1998-2008.
[2]. Česen MH, et al. Siramesine triggers cell death through destabilisation of mitochondria, but not lysosomes. Cell Death Dis. 2013;4(10):e818. Published 2013 Oct 3.
[3]. Ostenfeld MS, et al. Anti-cancer agent siramesine is a lysosomotropic detergent that induces cytoprotective autophagosome accumulation. Autophagy. 2008;4(4):487-499.
Siramesine (Lu 28-179) is a potent sigma-2 receptor agonist. Siramesine has a subnanomolar affinity for sigma-2 receptors (IC50=0.12 nM) and exhibits a 140-fold selectivity for sigma-2 receptors over sigma-1 receptors (IC50=17 nM). Siramesine triggers cell death through destabilisation of mitochondria, but not lysosomes. Anti-cancer activity[1][2][3].
体外研究 (In Vitro)
Siramesine displays the binding affinities: IC50 (sigma 1)=17 nM, IC50 (sigma 2)=0.12 nM, IC50 (5-HT1A)=21000 nM, IC50 (5-HT1A)=2000 nM, IC50 (D2)=800 nM, IC50 (alpha 1)=330 nM[1]. Siramesine (0-50μM; 8 hours) induces cell death in various cell lines (HaCaT, Hsc-4, HeLa and MCF-7, neuroblastoma cell line SH-SY5Y and glioblastoma cell line U-87MG)[2]. Siramesine (0-40 μM; 2-48 hours) activates caspases in HaCaT and in U-87MG cells[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
454.58
Formula
C30H31FN2O
CAS 号
147817-50-3
中文名称
西拉美新
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]. Perregaard J, et al. Sigma ligands with subnanomolar affinity and preference for the sigma 2 binding site. 1. 3-(omega-aminoalkyl)-1H-indoles. J Med Chem. 1995;38(11):1998-2008.
[2]. Česen MH, et al. Siramesine triggers cell death through destabilisation of mitochondria, but not lysosomes. Cell Death Dis. 2013;4(10):e818. Published 2013 Oct 3.
[3]. Ostenfeld MS, et al. Anti-cancer agent siramesine is a lysosomotropic detergent that induces cytoprotective autophagosome accumulation. Autophagy. 2008;4(4):487-499.
Regadenoson (CVT-3146) is a potent and selective A2A adenosine receptor agonist, with Kis of 290 and 1120 nM for rat and pig adenosine A2A receptor, respectively. Regadenoson is selective for the adenosine A2A receptor over adenosine A1 and A2B receptors, and shows 13-fold selectivity over the human adenosine A1 receptor. Regadenoson is a vasodilator stress agent has shifted the landscape of vasodilator myocardial perfusion imaging. Regadenoson increases blood-brain barrier (BBB) permeability in rodents[1][2][3].
Clinical Trial
分子量
390.35
Formula
C15H18N8O5
CAS 号
313348-27-5
中文名称
瑞加德松；类伽腺苷
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Palle VP, et al. Structure-affinity relationships of the affinity of 2-pyrazolyl adenosine analogues for the adenosine A2A receptor. Bioorg Med Chem Lett. 2002;12(20):2935-2939.
[2]. Golzar Y, et al. Regadenoson use in patients with chronic obstructive pulmonary disease: the state of current knowledge. Int J Chron Obstruct Pulmon Dis. 2014;9:129-137. Published 2014 Jan 22.
[3]. Jackson S, et al. The effect of regadenoson on the integrity of the human blood-brain barrier, a pilot study. J Neurooncol. 2017;132(3):513-519.
Lenvatinib (E7080) is an oral, multi-targeted tyrosine kinase inhibitor that inhibits VEGFR1-3, FGFR1-4, PDGFR, KIT, and RET, shows potent antitumor activities[1][2].
IC50 & Target[1][2][3]
VEGFR2
4 nM (IC50)
VEGFR3
5.2 nM (IC50)
VEGFR1
22 nM (IC50)
FGFR1
46 nM (IC50)
FGFR2
FGFR3
FGFR4
PDGFRα
51 nM (IC50)
PDGFRβ
39 nM (IC50)
c-Kit
100 nM (IC50)
RET
体外研究 (In Vitro)
Lenvatinib (E7080) has IC50s of 4, 5.2, 22 nM for VEGFR2 (KDR), VEGFR3 (Flt-4), and VEGFR1 (Flt-1), respectively. Lenvatinib inhibits PDGFRα, PDGFRβ, FGFR1, and KIT with IC50s of 51, 39, 46, and 100 nM, respectively[3].
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)
Lenvatinib (E7080) (100 mg/kg, p.o.) significantly inhibits local tumor growth at the m.f.p., and at the end of treatment, Lenvatinib mesylate also significantly inhibits metastasis to both regional lymph nodes and distant lung[3]. Lenvatinib (E7080) inhibits the growth of H146 tumor at 30 and 100 mg/kg (BID, QDx21) in a dose-dependent manner and causes tumor regression at 100 mg/kg in H146 xenograft model. IHC analysis with anti-CD31 antibody shows that lenvatinib at 100 mg/kg decreases microvessel density more than anti-VEGF antibody and STI571 treatment[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.
Clinical Trial
分子量
426.85
Formula
C21H19ClN4O4
CAS 号
417716-92-8
中文名称
乐伐替尼；仑伐替尼；乐法替尼
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Kudo M, et al. Lenvatinib versus Bay 43-9006 in first-line treatment of patients with unresectable hepatocellularcarcinoma: a randomised phase 3 non-inferiority trial. Lancet. 2018 Mar 24;391(10126):1163-1173.
[2]. Suyama K, et al. Lenvatinib: A Promising Molecular Targeted Agent for Multiple Cancers. Cancer Control. 2018 Jan-Dec;25(1):1073274818789361.
[3]. Matsui J, et al. E7080, a novel inhibitor that targets multiple kinases, has potent antitumor activities against stem cell factor producing human small cell lung cancer H146, based on angiogenesis inhibition. Int J Cancer. 2008, 122(3), 664-671.
[4]. Matsui J, et al. Multi-kinase inhibitor E7080 suppresses lymph node and lung metastases of human mammary breast tumor MDA-MB-231 via inhibition of vascular endothelial growth factor-receptor (VEGF-R) 2 and VEGF-R3 kinase. Clin Cancer Res. 2008, 14(17),545.
Cell Assay [1]
H146 (1.2×103 cells/50 μL/well) in SFM containing 0.5% BSA are cultured in 96-well multi-plates. After overnight culture at 37°C, SFM (150 μL/well) containing 0.5% FBS and several concentrations of SCF are added with or without several concentrations of compound. After culture for 72 hr, the ratios of surviving cells are measured by WST-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]
Female BALB/c nude mice (8-12 weeks old, 20-25 g) are maintained under clean-room conditions. H146 tumor cells (6.5×106) are implanted subcutaneously (s.c.) into the flank region of mice. Twelve days after inoculation, mice are randomized into control (n=12) and treatment (n=6 or n=5) groups and this point in time is identified as day 1. Lenvatinib and STI571, and VEGF neutralization antibody are suspended in 0.5% methylcellulose and saline, respectively, and administered orally twice a day for lenvatinib and STI571 and twice a week for antibody from day 1 to day 21. Tumor volume is measured on the indicated days and calculated. Antitumor activity is shown as a relative tumor volume (RTV=calculated tumor volume at indicated days/volume on day 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]. Kudo M, et al. Lenvatinib versus Bay 43-9006 in first-line treatment of patients with unresectable hepatocellularcarcinoma: a randomised phase 3 non-inferiority trial. Lancet. 2018 Mar 24;391(10126):1163-1173.
[2]. Suyama K, et al. Lenvatinib: A Promising Molecular Targeted Agent for Multiple Cancers. Cancer Control. 2018 Jan-Dec;25(1):1073274818789361.
[3]. Matsui J, et al. E7080, a novel inhibitor that targets multiple kinases, has potent antitumor activities against stem cell factor producing human small cell lung cancer H146, based on angiogenesis inhibition. Int J Cancer. 2008, 122(3), 664-671.
[4]. Matsui J, et al. Multi-kinase inhibitor E7080 suppresses lymph node and lung metastases of human mammary breast tumor MDA-MB-231 via inhibition of vascular endothelial growth factor-receptor (VEGF-R) 2 and VEGF-R3 kinase. Clin Cancer Res. 2008, 14(17),545.
SCH 58261 is a potent, selective and competitive antagonist of adenosine A2A receptor with an IC50 of 15 nM, and displays 323-, 53- and 100-fold more selective for A2A receptor than A1, A2B, and A3 receptors, respectively[1][2][3].
IC50 & Target
IC50: 15 nM (A2A receptor)[2]
体外研究 (In Vitro)
SCH 58261 (0 nM–10 µM; 7 days) decreases cell viability in a concentration-dependent in the NSCLC cell line H1975[4]. SCH58261 (25 μM; 72 hours) can inhibit the growth of CAF cells[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.
Cell Viability Assay[4]
Cell Line:
H1975 cells
Concentration:
10 nM-10 µM
Incubation Time:
7 days
Result:
Produced a concentration-dependent decrease in H1975 cell growth.
Cell Proliferation Assay[5]
Cell Line:
CAF cells
Concentration:
25 μM
Incubation Time:
72 hours
Result:
Inhibit the growth of CAF1 and CAF2 cells.
体内研究 (In Vivo)
SCH 58261 (2 mg/kg; i.p.; daily; for 20 days) causes a decrease in the tumor burden in a NSCLC mouse model[5]. SCH 58261 (5 mg/kg; i.p.; 3 times; every 3 hours; 10 minutes before haloperidol) partially decreases the haloperidol-induced catalepsy and the increase in the PENK mRNA expression in both dorsolateral and ventrolateral parts of the striatum at all three examined levels[6]. SCH 58261 diminishes the parkinsonian-like muscle rigidity and potentiates the effect of L-DOPA in rat model[7].
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:
4‒6 weeks old athymic nude mice (NCI) with PC9 cells xenograft[5]
Dosage:
2 mg/kg
Administration:
Intraperitoneal injection; daily; for 20 days
Result:
Decreased tumor growth.
分子量
345.36
Formula
C18H15N7O
CAS 号
160098-96-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Zocchi C, et al. Binding of the radioligand [3H]-SCH 58261, a new non-xanthine A2A adenosine receptor antagonist, to rat striatal membranes. Br J Pharmacol. 1996 Apr;117(7):1381-6.
[2]. Varani K, et al. Pharmacological and biochemical characterization of purified A2a adenosine receptors in human platelet membranes by [3H]-CGS 21680 binding. Br J Pharmacol. 1996 Apr;117(8):1693-701.
[3]. Xi J, et al. Adenosine A2A and A2B receptors work in concert to induce a strong protection against reperfusion injury in rat hearts. J Mol Cell Cardiol. 2009 Nov;47(5):684-90.
[4]. Kuzumaki N, et al. Multiple analyses of G-protein coupled receptor (GPCR) expression in the development of gefitinib-resistance in transforming non-small-cell lung cancer. PLoS One. 2012;7(10):e44368.
[5]. Mediavilla-Varela M, et al. Antagonism of adenosine A2A receptor expressed by lung adenocarcinoma tumor cells and cancer associated fibroblasts inhibits their growth. Cancer Biol Ther. 2013 Sep;14(9):860-8.
[6]. Wardas J, et al. SCH 58261, a selective adenosine A2A receptor antagonist, decreases the haloperidol-enhanced proenkephalin mRNA expression in the rat striatum. Brain Res. 2003 Jul 11;977(2):270-7.
[7]. Wardas J, et al. SCH 58261, an A(2A) adenosine receptor antagonist, counteracts parkinsonian-like muscle rigidity in rats. Synapse. 2001 Aug;41(2):160-71.
L-732138 is a selective, potent and competitive neurokinin-1 (NK-1) receptor antagonist with an IC50 of 2.3 nM. L-732138 has 200-fold more potent in cloned human NK-1 receptors than cloned rat NK-1 receptors, and has > 1000-fold more potent than human NK-2 and NK-3 receptors. L-732138 can reduce hyperalgesia and has antitumor action[1][2].
IC50 & Target[1][2]
NK1
2.3 nM (IC50)
体外研究 (In Vitro)
L-732138 (0 -100 µM; first doubling time; COLO 858, MEL HO and COLO 679 cells) treatment results in a concentration-dependent cytotoxicity. L-732138 inhibits cell growth with IC50 of 44.6 μM for COLO 858 cells, 76.3 μM for MEL HO cells and 64.2 μM for COLO 679 cells. L-732138 blocks substance P (SP) mitogen stimulation[1]. L-732,138 treatment results in a large number of apoptotic cells were found in COLO 858, MEL HO and COLO 679 melanoma cell lines. In DAPI-stained cultures, at IC50 concentration of 43.6% apoptotic cells for the three melanoma cell lines, whereas at IC100 concentration of 51.4 % apoptotic 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.
Cell Proliferation Assay[1]
Cell Line:
COLO 858, MEL HO and COLO 679 cells
Concentration:
0 µM, 20 µM, 40 µM, 60 µM, 80 µM, 100 µM
Incubation Time:
First doubling time
Result:
Resulted in a concentration-dependent cytotoxicity.
体内研究 (In Vivo)
L-732138 (10-4-10-2 mol/kg; intravenous injection; for 15 minutes; male Dunkin-Hartley guinea-pigs) treatment abolishes vagally-induced plasma exudation and significantly inhibits the enhancement by LPS. The LPS-enhanced vagally-induced plasma exudation is not completely inhibited by either L-732138 or SOD pretreatment alone, but is blocked by the combination of both pretreatments[3].
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:
Male Dunkin-Hartley guinea-pigs (350-500 g) injected with lipopolysaccharide (LPS)[3]
Dosage:
10-4 mol/kg , 10-3 mol/kg and 10-2 mol/kg
Administration:
Intravenous injection; for 15 minutes
Result:
Abolished the vagally-induced plasma leakage in tracheobronchial tissues, and dose-dependently inhibited the LPS enhanced vagally-induced plasma exudation in traceobronchial tissues.
分子量
472.38
Formula
C22H18F6N2O3
CAS 号
148451-96-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Muñoz M, et al. The NK-1 Receptor Antagonist L-732,138 Induces Apoptosis and Counteracts Substance P-Related Mitogenesis in Human Melanoma Cell Lines. Cancers (Basel). 2010 Apr 20;2(2):611-23.
[2]. Cascieri MA, et al. Characterization of the interaction of N-acyl-L-tryptophan benzyl ester neurokinin antagonists with the human neurokinin-1 receptor. J Biol Chem. 1994 Mar 4;269(9):6587-91.
[3]. Kuo HP, et al. Lipopolysaccharide enhances neurogenic plasma exudation in guinea-pig airways. Br J Pharmacol. 1998 Oct;125(4):711-6.
Cannabigerol, one of the major phytocannabinoids, behaves as a weak partial agonist at CB1 and CB2 receptors. Cannabigerol is also a relatively potent and highly effective TRPA1 agonist (EC50=0.7μM), a weak agonist at TRPV1 and TRPV2 (1.3 and 1.72 μM, respectively), and a potent TRPM8 (0.16 μM) and 5-HT1A receptor antagonist. Cannabigerol is a potent α2-adrenoceptor agonist (0.2 nM). Cannabigerol promotes apoptosis, stimulates reactive oxygen species (ROS) production, upregulates CHOP mRNA and reduces cell growth in CRC cells[1][2][3][4].
体外研究 (In Vitro)
Cannabigerol (CBG) antagonizes the 5-HT1A receptor agonist, R-(+)-8-hydroxy-2-(di-n-propylamino)tetralin (apparent KB=51.9 nM)[1]. In CHO cells stably expressing human receptors, Cannabigerol is a weak partial agonist of both CB1R- and CB2R-dependent inhibition of cAMP that displaying a low affinity for CB1R and comparatively higher affinity for CB2R (Ki= 1300 and 490 nM, respectively)[3]. Cannabigerol (1-30 μM; 3-48 hurs) reduces cell viability in human colorectal cancer (Caco-2) cells in a time- and serum protein concentration-dependent manner[3]. Cannabigerol (10 μM; 24 hours) induces apoptosis in colorectal cancer (Caco-2) cells[3].
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)
Cannabigerol (1-10 mg/kg; intraperitoneally; every day for 5 days; athymic female mice bearing HCT 116 cells) reduces colon carcinogenesis in vivo[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
316.48
Formula
C21H32O2
CAS 号
25654-31-3
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]. Cascio MG, et al. Evidence that the plant cannabinoid cannabigerol is a highly potent alpha2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist. Br J Pharmacol. 2010;159(1):129-141.
[2]. De Petrocellis L, et al. Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes. Br J Pharmacol. 2011;163(7):1479-1494.
[3]. Borrelli F, et al. Colon carcinogenesis is inhibited by the TRPM8 antagonist cannabigerol, a Cannabis-derived non-psychotropic cannabinoid. Carcinogenesis. 2014;35(12):2787-2797.
[4]. Zagzoog A, et al. In vitro and in vivo pharmacological activity of minor cannabinoids isolated from Cannabis sativa. Sci Rep. 2020;10(1):20405. Published 2020 Nov 23.
SR1078 is a selective agonist of retinoic acid receptor-related orphan receptor α/γ (RORα/RORγ). SR1078 directly binds to the ligand binding domain of RORα and RORγ and increases the transcriptional activity of these receptors, leading to stimulation of RORα/γ target gene transcription[1][2].
IC50 & Target
RORα/γ[1]
体外研究 (In Vitro)
SR1078 is a synthetic RORα/RORγ ligand. SR1078 modulates the conformation of RORγ in a biochemical assay and activates RORα and RORγ driven transcription. Furthermore, SR1078 stimulates expression of endogenous ROR target genes in HepG2 cells that express both RORα and RORγ. In a cell-based chimeric receptor Gal4 DNA-binding domain-NR ligand binding domain cotransfection assay, SR1078 significantly inhibits the constitutive transactivation activity of RORα and RORγ, but has no effect on the activity of FXR, LXRα and LXRβ. In a RORα cotransfection assay, treatment of cells with SR1078 (10 μM) results in a significant increase in transcription. Similarly, in the RORγ cotransfection assay, SR1078 treatment results in a stimulation of RORγ-dependent transcription activity[1]. SR1078 (2-10 μM; 24 hours) shows a dose-dependent increase in expression of A2BP1, CYP19A1, NLGN1, and IPTR1 in SH-SY5Y cells. EC50’s are in the range of 3-5 μM[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)
The pharmacokinetic properties of SR1078 are examined in mice and noted significant exposure. Plasma concentrations reach 3.6 μM 1h after a 10 mg/kg i.p. injection of SR1078 and sustained levels of above 800 nM even 8h after the single injection. These levels are sufficient to perform a proof-of-principle experiment to determine if SR1078 treatment would stimulate ROR target gene expression in an animal model. Mice are treated with SR1078 (10 mg/kg; i.p.) and 2h after the injection the livers are harvested and mRNA purified for assessment of G6Pase and FGF21 gene expression.T he expression of both FGF21 and G6Pase is significantly stimulated by SR1078 treatment vs. vehicle control[1]. SR1078 (10 mg/kg; i.p.) shows a significant 25% reduction in repetitive grooming behavior in the BTBR mice[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
431.25
Formula
C17H10F9NO2
CAS 号
1246525-60-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Wang Y, et al. Identification of SR1078, a synthetic agonist for the orphan nuclear receptors RORα and RORγ. ACS Chem Biol. 2010 Nov 19;5(11):1029-34.
[2]. Wang Y, Billon C, Walker JK, Burris TP. Therapeutic Effect of a Synthetic RORα/γ Agonist in an Animal Model of Autism. ACS Chem Neurosci. 2016;7(2):143-148.
Kinase Assay [1]
The ALPHA screen assays are performed. Assays are performed in triplicate in white opaque 384-well plates under green light conditions (<100 lux) at room temperature. the final assay volume is 20 μl. all dilutions are made in buffer (100 mm nacl, 25 hepes, 0.1% (w>[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 Assay [1]
HEK293 cells are maintained in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% (v/v) fetal bovine serum at 37°C under 5% CO2. HepG2 cells are maintained and routinely propagated in minimum essential medium supplemented with 10% (v/v) fetal bovine serum at 37°C under 5% CO2. In experiments where lipids and sterols are depleted, cells are maintained on charcoal treated serum (10% (v/v) fetal bovine serum) and treated with 7.5 μM lovastatin and 100 μM mevalonic acid. 24 h prior to transfection, HepG2 or HEK293 cells are plated in 96-well plates at a density of 15×103 cells/well. Transfections are performed using LipofectamineTM 2000. 16 h post-transfection, the cells are treated with vehicle or SR1078. 24 h post-treatment, the luciferase activity is measured using the Dual-GloTM luciferase assay system. The experiments are repeated at least three times[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]
Mice[1] Plasma levels of SR1078 are evaluated in C57BL6 mice (n=3 per time point) administered by i.p. injection. After 1, 2, 4, and 8h blood is taken. In the 2h time point liver is taken for target gene analysis. Plasma is generated using standard centrifugation techniques, and the plasma and tissues are frozen at −80°C. Plasma and tissues are mixed with acetonitrile (1:5 (v/v) or 1:5 (w/v), respectively), sonicated with a probe tip sonicator, and analyzed for drug levels by liquid chromatography/tandem mass spectrometry.
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]. Wang Y, et al. Identification of SR1078, a synthetic agonist for the orphan nuclear receptors RORα and RORγ. ACS Chem Biol. 2010 Nov 19;5(11):1029-34.
[2]. Wang Y, Billon C, Walker JK, Burris TP. Therapeutic Effect of a Synthetic RORα/γ Agonist in an Animal Model of Autism. ACS Chem Neurosci. 2016;7(2):143-148.
Lenvatinib mesylate (E7080 mesylate), an oral, multi-targeted tyrosine kinase inhibitor that inhibits VEGFR1-3, FGFR1-4, PDGFR, KIT, and RET, shows potent antitumor activities[1][2].
IC50 & Target[1][2][3]
VEGFR1
22 nM (IC50)
VEGFR2
4 nM (IC50)
VEGFR3
5.2 nM (IC50)
FGFR1
46 nM (IC50)
FGFR2
FGFR3
FGFR4
PDGFRα
51 nM (IC50)
PDGFRβ
39 nM (IC50)
c-Kit
100 nM (IC50)
RET
体外研究 (In Vitro)
Lenvatinib mesylate (E7080 mesylate) has IC50s of 4, 5.2, 22 nM for VEGFR2(KDR), VEGFR3(Flt-4), and VEGFR1/Flt-1, respectively. Lenvatinib inhibits PDGFRα, PDGFRβ, FGFR1, and KIT with IC50s of 51, 39, 46, 100 nM, respectively[3].
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)
Lenvatinib mesylate (E7080 mesylate) (100 mg/kg, p.o.) is administeredand bevacizumab significantly inhibits local tumor growth at the m.f.p., and at the end of treatment, Lenvatinib mesylate also significantly inhibits metastasis to both regional lymph nodes and distant lung[3]. Lenvatinib mesylate (E7080 mesylate) inhibits the growth of H146 tumor at 30 and 100 mg/kg (BID, QDx21) in a dose-dependent manner and causes tumor regression at 100 mg/kg in H146 xenograft model. IHC analysis with anti-CD31 antibody shows that lenvatinib at 100 mg/kg decreases microvessel density more than anti-VEGF antibody and imatinib treatment[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.
Clinical Trial
分子量
522.96
Formula
C22H23ClN4O7S
CAS 号
857890-39-2
中文名称
乐伐替尼甲酸盐；仑伐替尼甲酸盐；乐法替尼甲酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
4°C, sealed storage, away from moisture and light
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
溶解性数据
In Vitro:
DMSO : 7.35 mg/mL (14.05 mM; Need ultrasonic)
配制储备液
浓度溶剂体积质量
1 mg
5 mg
10 mg
1 mM
1.9122 mL
9.5610 mL
19.1219 mL
5 mM
0.3824 mL
1.9122 mL
3.8244 mL
10 mM
0.1912 mL
0.9561 mL
1.9122 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 (sealed storage, away from moisture and light)。-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。
参考文献
[1]. Kudo M, et al. Lenvatinib versus sorafenib in first-line treatment of patients with unresectable hepatocellularcarcinoma: a randomised phase 3 non-inferiority trial. Lancet. 2018 Mar 24;391(10126):1163-1173.
[2]. Suyama K, et al. Lenvatinib: A Promising Molecular Targeted Agent for Multiple Cancers. Cancer Control. 2018 Jan-Dec;25(1):1073274818789361.
[3]. 3.Matsui J, et al. Multi-kinase inhibitor E7080 suppresses lymph node and lung metastases of human mammary breast tumor MDA-MB-231 via inhibition of vascular endothelial growth factor-receptor (VEGF-R) 2 and VEGF-R3 kinase. Clin Cancer Res. 2008, 14(17),545.
[4]. Matsui J, et al. E7080, a novel inhibitor that targets multiple kinases, has potent antitumor activities against stem cell factor producing human small cell lung cancer H146, based on angiogenesis inhibition. Int J Cancer. 2008, 122(3), 664-671.
Furosemide is a potent and orally active inhibitor of Na+/K+/2Cl– (NKCC) cotransporter, NKCC1 and NKCC2[1]. Furosemide is also a GABAA receptors antagonist and displays 100-fold selectivity for α6-containing receptors than α1-containing receptors. Furosemide acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema[2].
IC50 & Target
IC50: NKCC1 and NKCC2[1]IC50: GABAA receptors[2]
体外研究 (In Vitro)
Furosemide (500 µM; 72-96 hours) significantly changes the proliferation rates in MKN45 cells (the poorly differentiated human gastric adenocarcinoma cell line). however, it has no effects on MKN28 cells (the moderately differentiated human gastric adenocarcinoma cell line). The growth rate of MKN45 cells is larger than that of MKN28 cells[4].Furosemide (10 µM, 30 µM, 100 µM; 45 min exposure) significantly decreases cation channel activity and [Ca(2+)](i) in human erythrocytes drawn from healthy individuals. Tert-butylhydroperoxide similarly enhances the non-selective cation channels activity, increases [Ca(2+)](i) and triggered cell membrane scrambling, however, the effects is significantly blunted by furosemide again[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.
体内研究 (In Vivo)
Furosemide (intraperitoneal injection; 100 mg/kg; single dose) is injected after kanamycin (KM) (1000 mg/kg) to creat a deaf mouse model in C57BL/6 mouse. After injection, hearing loss and cochlear hair cell damage are evaluated on day 1, day 2 and day 3, respectively. The hearing is markedly deteriorated even from the next day (Day-1 group), OHCs (outer hair cell) morphology of apical, middle and basal turns are disorganized in mice on day3[3].
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
330.74
Formula
C12H11ClN2O5S
CAS 号
54-31-9
中文名称
呋塞米；呋喃苯胺酸；速尿；利尿磺胺；速尿灵
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. C M Gillen, et al. Molecular cloning and functional expression of the K-Cl cotransporter from rabbit, rat, and human. A new member of the cation-chloride cotransporter family. J Biol Chem. 1996 Jul 5;271(27):16237-44.
[2]. S A Thompson, et al. Residues in transmembrane domains I and II determine gamma-aminobutyric acid type AA receptor subtype-selective antagonism by Furosemide sodium. Mol Pharmacol. 1999 Jun;55(6):993-9.
[3]. Shin Hye Kim, et al. Novel Peptide Vaccine GV1001 Rescues Hearing in Kanamycin/Furosemide sodium-Treated Mice. Front Cell Neurosci. 2018 Jan 19;12:3.
[4]. Atsushi Shiozaki , et al. Furosemide sodium, a blocker of Na+/K+/2Cl- cotransporter, diminishes proliferation of poorly differentiated human gastric cancer cells by affecting G0/G1 state. J Physiol Sci. 2006 Dec;56(6):401-6.
[5]. Yuliya V Kucherenko, et al.Inhibitory effect of Furosemide sodium on non-selective voltage-independent cation channels in human erythrocytes.Cell Physiol Biochem. 2012;30(4):863-75.
SU4984 is a protein tyrosine kinase inhibitor, with an IC50 of 10-20 μM for fibroblast growth factor receptor 1 (FGFR1). SU4984 is also inhibits platelet-derived growth factor receptor, and insulin receptor. SU4984 can be used for the research of cancer[1][2][3].
IC50 & Target[1]
FGFR1
10-20 μM (IC50)
体外研究 (In Vitro)
SU4984 (5-100 μM; 5 min) inhibits the kinase activity of FGFR1K with an IC50 of 10-20 μM in the presence of 1 mM adenosine triphosphate (ATP)[1]. SU4984 (10-90 μM; 5 min) inhibits the autophosphorylation of FGFR1 induced by aFGF in NIH 3T3 cells, with an IC50 of 20-40 μM[1]. SU4984 (5 μM) substantially reduces tyrosine phosphorylation of the wild-type receptor and reduces 50% phosphorylation of constitutive C2 KIT[2]. SU4984 (1-10 μM; 6 days) kills the C2 and P815 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
333.38
Formula
C20H19N3O2
CAS 号
186610-89-9
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]. Mohammadi M, et, al. Structures of the tyrosine kinase domain of fibroblast growth factor receptor in complex with inhibitors. Science. 1997 May 9;276(5314):955-60.
[2]. Ma Y, et, al. Indolinone derivatives inhibit constitutively activated KIT mutants and kill neoplastic mast cells. J Invest Dermatol. 2000 Feb;114(2):392-4.
ELN-441958 is a potent, neutral antagonist of B1 receptor, inhibits the binding of the B1 agonist ligand [3H]DAKD to IMR-90 cells with Ki of 0.26 nM. ELN-441958 is highly selective for B1 over B2 receptors, and >500/ 2000-fold selective for the B1 over μ/δ-opioid receptor. IC50 value: 0.26 nM (Ki) Target: B1 Receptor in vitro: ELN-441958 is a novel small molecule bradykinin B1 receptor antagonist, based on the inhibition of agonist-induced increases in intracellular calcium in native and recombinant cells. ELN-441958 does not inhibit the activation of the human bradykinin B2 receptor at concentrations up to 10 μM, showing that it is highly selective for B1 over B2 receptors. ELN-441958 also displays good selectivity for B1 over other receptors examined in a broad screening panel. It is >500-fold and >2000-fold selective for the B1 receptor over the human μ- and δ-opioid receptor, the most potent off-target activity identified. In IMR-90 cells expressing the native human B1 receptor, ELN-441958 produced a concentration-dependent antagonism of the DAKD-induced calcium mobilization with a KB of 0.12 nM. [1] in vivo: ELN-441958 is essentially completely absorbed and produces high plasma levels after oral administration in rhesus monkeys.ELN-441958 has a moderate clearance and volume of distribution in both species following i.v. administration, consistent with the high metabolic stability in rat, rhesus, and human microsomes. ELN-441958 has high oral exposure and moderate plasma half-lives in rats and rhesus monkeys. The oral availability of ELN441958 in rats was 57%. ELN-441958 dose-dependently reduced carrageenan-induced thermal hyperalgesia in a rhesus monkey tail-withdrawal model, with an ED50 3 mg/kg s.c. [1]
分子量
501.02
Formula
C29H29ClN4O2
CAS 号
913064-47-8
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Hawkinson JE, et al. Pharmacological, pharmacokinetic, and primate analgesic efficacy profile of the novel bradykinin B1 Receptor antagonist ELN441958. J Pharmacol Exp Ther.2007 Aug;322(2):619-630.
L748337 is a potent β3-adrenergic receptor antagonist and displays selectivity over β1 and β2 receptors. The Ki values of L748337 for β3-, β2- and β1-adrenoceptors are 4.0 nM, 204 nM and 390 nM, respectively[1]. L748337 couples predominantly to Gi to activate MAPK signaling and increases phosphorylation of Erk1/2 with pEC50 value of 11.6[2]. L748337 can be used for the research of cancer, nonalcoholic fatty liver disease (NAFLD), and cardiovascular related diseases[1][2][3].
IC50 & Target[1]
Beta-3 adrenergic receptor
4 nM (Ki)
Beta-2 adrenergic receptor
204 nM (Ki)
Beta-1 adrenergic receptor
390 nM (Ki)
体外研究 (In Vitro)
L748337 (1 μM) inhibits iNOS expression in B16F10 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.
体内研究 (In Vivo)
L-748337 (intraperitoneal injection; 5 mg/kg; beginning 10 days until D18) decreases the growth of melanoma induced by B16F10 cell inoculation and decreases tumor vasculature in mice[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:
Fifty male C57BL/6 J mice (8 weeks of age) bearing syngeneic B16F10 cell[1]
Dosage:
5 mg/kg
Administration:
Beginning 10 days until D18
Result:
Exhibited anti-cancer effects.
分子量
497.61
Formula
C26H31N3O5S
CAS 号
244192-94-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. S Neidhold, et al. The function of alpha- and beta-adrenoceptors of the saphenous artery in caveolin-1 knockout and wild-type mice. Br J Pharmacol. 2007 Feb;150(3):261-70.
[2]. Masaaki Sato, et al. The beta3-adrenoceptor agonist 4-[[(Hexylamino)carbonyl]amino]-N-[4-[2-[[(2S)-2-hydroxy-3-(4-hydroxyphenoxy)propyl]amino]ethyl]-phenyl]-benzenesulfonamide (L755507) and antagonist (S)-N-[4-[2-[[3-[3-(acetamidomethyl)phenoxy]-2-hydroxypropyl]amino]-ethyl]phenyl]benzenesulfonamide (L748337) activate different signaling pathways in Chinese hamster ovary-K1 cells stably expressing the human beta3-adrenoceptor. Mol Pharmacol. 2008 Nov;74(5):1417-28.
[3]. Ziwen Wang, et al. The protective effects of the β3 adrenergic receptor agonist BRL37344 against liver steatosis and inflammation in a rat model of high-fat diet-induced nonalcoholic fatty liver disease (NAFLD). Mol Med. 2020 Jun 5;26(1):54.
PB28 dihydrochloride, a cyclohexylpiperazine derivative, is a high affinity and selective sigma 2 (σ2) receptor agonist with a Ki of 0.68 nM. PB28 dihydrochloride is also a σ1 antagonist with a Ki of 0.38 nM. PB28 dihydrochloride is less affinity for other receptors. PB28 dihydrochloride inhibits electrically evoked twitch in guinea pig bladder and ileum with EC50 values of 2.62 μM and 3.96 μM, respectively. PB28 dihydrochloride can modulate SARS-CoV-2-human protein-protein interaction. PB28 dihydrochloride induces caspase-independent apoptosis and has antitumor activity[1][2][3][4][5].
体外研究 (In Vitro)
PB28 (15-25 nM; 24-48 hours; MCF7 and MCF7 ADR cells) dihydrochloride treatment shows an accumulation in the G0-G1 phase for MCF7 and MCF7 ADR cells that are time and concentration independent[1]. PB28 dihydrochloride has a higher σ2 receptor affinity expressed as Ki (0.28 nM and 0.17 nM in MCF7 and MCF7 ADR cells, respectively) than σ1 receptor affinity (13.0 nMand 10.0 nM, respectively)[1]. PB28 dihydrochloride inhibits cell growth of MCF7 and MCF7 ADR cells with IC50s of 25 nM and 15 nM, respectively after 2-day treatment[1]. PB28 dihydrochloride induces apoptosis through a caspase-independent pathway[1]. PB28 dihydrochloride also reduces P-gp expression in a concentration- and time-dependent manner (approximately 60% in MCF7 and 90% in MCF7 ADR)[1]. PB28 dihydrochloride displays antiproliferative and cytotoxic effects in both C6 rat glioma and SK-N-SH human neuroblastoma cell lines[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:
MCF7 and MCF7 ADR cells
Concentration:
25 nM and 15 nM
Incubation Time:
24 hours, 48 hours
Result:
Showed an accumulation in the G0-G1 phase for MCF7 and MCF7 ADR cells that were time and concentration independent.
体内研究 (In Vivo)
PB28 (10.7 mg/mL; intraperitoneal injection; daily; for two weeks; C57BL/6 female mice) dihydrochloride treatment inhibits tumor growth in Panc02 tumor burden mice. PB28 also conferres a survival advantage for mice[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 Model:
C57BL/6 female mice (10 weeks old) injected with Panc02 cells[2]
Dosage:
10.7 mg/mL
Administration:
Intraperitoneal injection; daily; for two weeks
Result:
Inhibited tumor growth in Panc02 tumor burden mice.
分子量
443.49
Formula
C24H40Cl2N2O
CAS 号
172907-03-8
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Amalia Azzariti, et al. Cyclohexylpiperazine Derivative PB28, a sigma2 Agonist and sigma1 Antagonist Receptor, Inhibits Cell Growth, Modulates P-glycoprotein, and Synergizes With Anthracyclines in Breast Cancer. Mol Cancer Ther. 2006 Jul;5(7):1807-16.
[2]. Maria Laura Pati, et al. Sigma-2 Receptor Agonist Derivatives of 1-Cyclohexyl-4-[3-(5-methoxy-1,2,3,4-tetrahydronaphthalen-1-yl)propyl]piperazine (PB28) Induce Cell Death via Mitochondrial Superoxide Production and Caspase Activation in Pancreatic Cancer. BMC Cancer. 2017 Jan 13;17(1):51.
[3]. Nicola A Colabufo, et al. A New Method for Evaluating sigma(2) Ligand Activity in the Isolated Guinea-Pig Bladder. Naunyn Schmiedebergs Arch Pharmacol. 2003 Aug;368(2):106-12.
[4]. Francesco Berardi, et al. Exploring the Importance of Piperazine N-atoms for sigma(2) Receptor Affinity and Activity in a Series of Analogs of 1-cyclohexyl-4-[3-(5-methoxy-1,2,3,4-tetrahydronaphthalen-1-yl)propyl]piperazine (PB28). J Med Chem. 2009 Dec 10;52(23):7817-28.
[5]. David E Gordon, et al. A SARS-CoV-2-Human Protein-Protein Interaction Map Reveals Drug Targets and Potential Drug-Repurposing. bioRxiv. 2020 Mar 22;2020.03.22.002386.
CITCO 是一种组成型雄甾烷 (Constitutive androstane) 受体激动剂，抑制脑肿瘤干细胞 (BTSCs) 的生长和扩增。CITCO 是一种咪唑并噻唑衍生物，其作为人 CAR 的选择性激动剂起作用。CITCO 对于孕烷 X 受体 (PXR) 的 EC50 为 49 nM，并且对其他核受体没有活性。
CITCO Chemical Structure
CAS No. : 338404-52-7
规格
价格
是否有货
数量
10 mM * 1 mL in DMSO
￥1845
In-stock
5 mg
￥1675
In-stock
10 mg
￥2680
In-stock
25 mg
￥5360
In-stock
50 mg
￥8580
In-stock
100 mg
询价
200 mg
询价
* Please select Quantity before adding items.
CITCO 相关产品
•相关化合物库:
Bioactive Compound Library Plus
Apoptosis Compound Library
Anti-Cancer Compound Library
Targeted Diversity Library
生物活性
CITCO, an imidazothiazole derivative, is a selective Constitutive androstane receptor (CAR) agonist. CITCO inhibits growth and expansion of brain tumour stem cells (BTSCs) and has an EC50 of 49 nM over pregnane X receptor (PXR), and no activity on other nuclear receptors[1].
IC50 & Target
CAR, PXR[1]
体外研究 (In Vitro)
CITCO (1-50 μM; 48 hours) results in a dose-dependent inhibition of viable cell count and proliferation in both T98G and U87MG glioma and BTSCs[1]. CITCO (2.5, 5 μM; 48 hours) induces cell cycle arrest differentially in different BTSCs in culture, but not in normal astrocytes[1]. CITCO (2.5-10 μM; 48 hours) induces apoptosis in BTSCs in culture in dose dependently, but not in normal astrocytes[1]. CITCO (0-25 μM; 48 hours) causes the T98G and U87MG glioma and BTSCs expressing very low levels of CAR protein that increased significantly[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 Proliferation Assay[1]
Cell Line:
T98G, U87MG, DB29 and DB33 human glioma cells, astrocytes
Concentration:
1, 2.5, 5, 10, 25, 50 μM
Incubation Time:
48 hours
Result:
Resulted in a dose-dependent inhibition of viable cell count and proliferation.
Cell Cycle Analysis[1]
Cell Line:
The T98G, U87MG, DB29 and DB33 glioma cells
Concentration:
2.5, 5 μM
Incubation Time:
48 hours
Result:
Induced cell cycle arrest differentially in different BTSCs in culture.
Apoptosis Analysis[1]
Cell Line:
The T98G, U87MG, DB29 and DB33 glioma cells
Concentration:
2.5, 5 or 10 μM
Incubation Time:
48 hours
Result:
Increased the levels of Annexin V-positive apoptotic cells in dose dependently.
Western Blot Analysis[1]
Cell Line:
T98G, U87MG, DB29 and DB33 glioma cells
Concentration:
0 to 25 μM
Incubation Time:
48 hours
Result:
The T98G, U87MG glioma and BTSCs expressed very low levels of CAR protein that increased significantly.
体内研究 (In Vivo)
CITCO (intraperitoneal; on days 22, 24, 26, 30 and 36) with 25 μg results a significant decrease in tumour growth, which further decreases to an undetectable level after treatment with 100 μg CITCO [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:
Six- to eight-week-old male athymic nude mice[1]
Dosage:
25 or 100 μg
Administration:
Intraperitoneal; on days 22, 24, 26, 30 and 36
Result:
Decreased tumour growth.
分子量
436.74
Formula
C19H12Cl3N3OS
CAS 号
338404-52-7
运输条件
Room temperature in continental US; may vary elsewhere.
BA 1 TFA is a potent agonist for the bombesin (BB) family of receptors. BA1 binds with high affinity to Bombesin receptor subtype-3 (BRS3), gastrin releasing peptide receptor (GRPR), neuromedin B receptor (NMBR) with IC50s of 6, 0.4, 2.5 nM[1].
2. Calculate the overall charge of the entire peptide according to the following table:
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3. Recommended solution:
Overall charge of peptide
Details
Negative (<0)
1. Try to dissolve the peptide in water first. 2. If water fails, add NH4OH (<50 μL). 3. If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (>0)
1. Try to dissolve the peptide in water first. 2. If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3. If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1. Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2. For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. Terry W Moody, et al. ML-18 is a non-peptide bombesin receptor subtype-3 antagonist which inhibits lung cancer growth. Peptides. 2015 Feb;64:55-61.
PU02, a derivative of 6-MP (HY-13677), is a negative allosteric modulator (NAM) of 5-HT3 receptor, with IC50 values of 0.36 and 0.73 μM in HEK293 cells transfected with human 5-HT3A and 5-HT3AB receptors respectively[1][2].
IC50 & Target[1]
5-HT3A Receptor
0.36 μM (IC50)
5-HT 3 AB
0.73 μM (IC50)
体外研究 (In Vitro)
PU02 (NMMP) (0-200 μM) leads to a steady decrease in cell viability of HepG2 cells (IC50=48.585 μM). PU02 (NMMP) shows less toxicity on L02 cells than did 6-MP after 48 h of treatment[2]. PU02 (NMMP) at 6.25 or 25 μM exhibits inhibitory effects on the viability of the tested cell lines, including SMMC-7721, MDA-MB-231, RKO and HCT-8 cells[2]. PU02 (NMMP) induces cell cycle arrest at the G2/M phase. PU02 (NMMP) downregulats the expression of cyclin B1/D1 and CDK4 in a time-dependent manner in HepG2 cells,but the expression of cyclin E is not affected[2]. PU02 (NMMP)-treated cells exhibits a significant increase in caspase-3 cleavage, suggesting enhanced apoptotic activity[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.
Apoptosis Analysis[2]
Cell Line:
HepG2 cells.
Concentration:
6.26, 12.5, 25, 50 μM.
Incubation Time:
6, 12, 24, 36 h.
Result:
Induced mitochondria-dependent apoptosis.
分子量
292.36
Formula
C16H12N4S
CAS 号
313984-77-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Sarah M Trattnig, et al. Discovery of a novel allosteric modulator of 5-HT3 receptors: inhibition and potentiation of Cys-loop receptor signaling through a conserved transmembrane intersubunit site. J Biol Chem. 2012 Jul 20;287(30):25241-54.
[2]. Xiao-Guang Yang, et al. 6-[(1-naphthylmethyl)sulfanyl]-9H-purine induces G2/M phase arrest and apoptosis in human hepatocellular carcinoma HepG2 cells. Eur J Pharmacol. 2012 Nov 15;695(1-3):27-33.
PB28 is a cyclohexylpiperazine derivative and a high affinity and selective sigma 2 (σ2) receptor agonist with a Ki of 0.68 nM. PB28 is also a σ1 antagonist with a Ki of 0.38 nM. PB28 is less affinity for other receptors. PB28 inhibits electrically evoked twitch in guinea pig bladder and ileum with EC50 values of 2.62 μM and 3.96 μM, respectively. PB28 can modulate SARS-CoV-2-human protein-protein interaction. PB28 induces caspase-independent apoptosis and has antitumor activity[1][2][3][4][5].
PB28 (15-25 nM; 24-48 hours; MCF7 and MCF7 ADR cells) treatment shows an accumulation in the G0-G1 phase for MCF7 and MCF7 ADR cells that are time and concentration independent[1]. PB28 has a higher σ2 receptor affinity expressed as Ki (0.28 nM and 0.17 nM in MCF7 and MCF7 ADR cells, respectively) than σ1 receptor affinity (13.0 nMand 10.0 nM, respectively)[1]. PB28 inhibits cell growth of MCF7 and MCF7 ADR cells with IC50s of 25 nM and 15 nM, respectively after 2-day treatment[1]. PB28 induces apoptosis through a caspase-independent pathway[1]. PB28 also reduces P-gp expression in a concentration- and time-dependent manner (approximately 60% in MCF7 and 90% in MCF7 ADR)[1]. PB28 displays antiproliferative and cytotoxic effects in both C6 rat glioma and SK-N-SH human neuroblastoma cell lines[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Cycle Analysis[1]
Cell Line:
MCF7 and MCF7 ADR cells
Concentration:
25 nM and 15 nM
Incubation Time:
24 hours, 48 hours
Result:
Showed an accumulation in the G0-G1 phase for MCF7 and MCF7 ADR cells that were time and concentration independent.
体内研究 (In Vivo)
PB28 (10.7 mg/mL; intraperitoneal injection; daily; for two weeks; C57BL/6 female mice) treatment inhibits tumor growth in Panc02 tumor burden mice. PB28 also conferres a survival advantage for mice[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
C57BL/6 female mice (10 weeks old) injected with Panc02 cells[2]
Dosage:
10.7 mg/mL
Administration:
Intraperitoneal injection; daily; for two weeks
Result:
Inhibited tumor growth in Panc02 tumor burden mice.
分子量
370.57
Formula
C24H38N2O
CAS 号
172906-90-0
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]. Amalia Azzariti, et al. Cyclohexylpiperazine Derivative PB28, a sigma2 Agonist and sigma1 Antagonist Receptor, Inhibits Cell Growth, Modulates P-glycoprotein, and Synergizes With Anthracyclines in Breast Cancer. Mol Cancer Ther. 2006 Jul;5(7):1807-16.
[2]. Maria Laura Pati, et al. Sigma-2 Receptor Agonist Derivatives of 1-Cyclohexyl-4-[3-(5-methoxy-1,2,3,4-tetrahydronaphthalen-1-yl)propyl]piperazine (PB28) Induce Cell Death via Mitochondrial Superoxide Production and Caspase Activation in Pancreatic Cancer. BMC Cancer. 2017 Jan 13;17(1):51.
[3]. Nicola A Colabufo, et al. A New Method for Evaluating sigma(2) Ligand Activity in the Isolated Guinea-Pig Bladder. Naunyn Schmiedebergs Arch Pharmacol. 2003 Aug;368(2):106-12.
[4]. Francesco Berardi, et al. Exploring the Importance of Piperazine N-atoms for sigma(2) Receptor Affinity and Activity in a Series of Analogs of 1-cyclohexyl-4-[3-(5-methoxy-1,2,3,4-tetrahydronaphthalen-1-yl)propyl]piperazine (PB28). J Med Chem. 2009 Dec 10;52(23):7817-28.
[5]. David E Gordon, et al. A SARS-CoV-2-Human Protein-Protein Interaction Map Reveals Drug Targets and Potential Drug-Repurposing. bioRxiv. 2020 Mar 22;2020.03.22.002386.
BA 1 is a potent agonist for the bombesin (BB) family of receptors. BA 1 binds with high affinity to Bombesin receptor subtype-3 (BRS3), gastrin releasing peptide receptor (GRPR), neuromedin B receptor (NMBR) with IC50s of 6, 0.4, 2.5 nM[1].
体外研究 (In Vitro)
BA 1 (0.1 μM) significantly increases FAK tyrosine phosphorylation in BRS-3 transfected NCI-H1299 cells[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
1133.30
Formula
C9H19FN3O2VWY
CAS 号
183241-31-8
Sequence Shortening
YQWAV{Bal}HF{Nle}-NH2
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.
Solvent & Solubility
In Vitro:
H2O
Peptide Solubility and Storage Guidelines:
1. Calculate the length of the peptide.
2. Calculate the overall charge of the entire peptide according to the following table:
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3. Recommended solution:
Overall charge of peptide
Details
Negative (<0)
1. Try to dissolve the peptide in water first. 2. If water fails, add NH4OH (<50 μL). 3. If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (>0)
1. Try to dissolve the peptide in water first. 2. If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3. If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1. Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2. For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. Terry W Moody, et al. ML-18 is a non-peptide bombesin receptor subtype-3 antagonist which inhibits lung cancer growth. Peptides. 2015 Feb;64:55-61.
