Boc-NH-PEG11-OH is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs[1].
IC50 & Target
PEGs
体外研究 (In Vitro)
PROTACs contain two different ligands connected by a linker; one is a ligand for an E3 ubiquitin ligase and the other is for the target protein. PROTACs exploit the intracellular ubiquitin-proteasome system to selectively degrade target proteins[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
601.72
Formula
C27H55NO13
CAS 号
1556847-53-0
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]. An S, et al. Small-molecule PROTACs: An emerging and promising approach for the development of targeted therapy drugs. EBioMedicine. 2018 Oct;36:553-562
IL-17A modulator-1 is a IL-17A modulator, extracted from patent WO2021239743+A1, example 9. IL-17A modulator-1 inhibits the biological action of IL-17A with a pIC50 of 8.2. IL-17A modulator-1 can be used for the research of diseases or disorders associated with modulation of IL-17A activity including diseases with an immune component or autoimmune pathol, cancer and neurodegenerative disorders[1].
IC50 & Target[1]
IL-17A
8.2 (pIC50)
分子量
561.63
Formula
C33H31N5O4
CAS 号
2748749-29-1
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]. Barrie Phillip MARTIN, et al. Preparation of amino acid amides as IL-17A modulators. WO2021239743 A1.
CHR-6494 TFA is a potent inhibitor of haspin, with an IC50 of 2 nM. CHR-6494 TFA inhibits histone H3T3 phosphorylation. CHR-6494 TFA induces the apoptosis of cancer cells, including melanoma and breast cancer. CHR-6494 TFA can be used in the research of cancer[1][2][3].
IC50 & Target[1]
haspin
2 nM (IC50)
体外研究 (In Vitro)
CHR-6494 (TFA; 0-105 nM; 72 hours) dose-dependently inhibits the growth of cancer cells, such as HCT-116, HeLa, MDA-MB-231, and Wi-38 cells, with IC50s of 500 nM, 473 nM, 752 nM and 1059 nM, respectively[1]. CHR-6494 (TFA; 500 nM) produces a mitotic catastrophe with abnormal morphology of the mitotic spindle and centrosome amplification, and upregulates the spindle assembly checkpoint protein BUB1 and the marker of mitotic arrest cyclin B1[1]. CHR-6494 (TFA; 0, 0.5, 1.0 μM; 24 to 36 h) is an inhibitor of angiogenesis in the ex vivo chicken embryo aortic arch ring assay[1]. CHR-6494 (TFA) exhibits inhibitory activities against melanoma cell lines, including BRAFV600E mutants, NRAS mutants, and wild type cells, with IC50s ranging from 396 nM to 1229 nM[2]. CHR-6494 (TFA; 300 nM and 600 nM; 72 hours) induces apoptosis, increases caspase 3/7 activity by 3- and 6-fold, respectively in COLO-792 cells, and to 8.5- and 16-fold in RPMI-7951 melanoma cells[2]. CHR-6494 (TFA; 50, 200 nM; 1 week) enhances the antiproliferative effects of MLN8237 in MDA-MB-231, SKBR3 breast cancer cells[3]. CHR-6494 (TFA; 200 nM; 72 hours) enhances the apoptosis of MDA-MB-231 and SKBR3 cells when combined with MLN8237[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)
CHR-6494 (TFA; 50 mg/kg; i.p. in two cycles of five consecutive days for 15 days) inhibits the growth of tumor in nude mice bearing HCT-116 human colorectal cancer cells[1]. CHR-6494 (TFA; 20 mg/kg; intraperitoneal injection for 15 consecutive days) inhibits the tumor growth in nude mice bearing MDA-MB-231 xenograft tumors[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Male 4-5 weeks old athymic nu/nu mice harboring HCT-116 cells xenograft tumor with a tumor volume of 200 mm3[1]
Dosage:
50 mg/kg (diluted in a solution of 10% DMSO/20% 2-hydroxypropyl-b-cyclodextrin)
Administration:
i.p. in two cycles of five consecutive days for 15 days
Result:
Dose-dependent tumor growth inhibition was demonstrated. Did not change the body weight of mice.
20 mg/kg in a final formulation in 10% DMSO/20% 2‐hydroxypropyl‐β‐cyclodextrin
Administration:
i.p. for 15 consecutive days
Result:
Inhibited the tumor volume and weight compared with the control group in nude mice bearing MDA-MB-231 xenograft tumors. Enhanced the tumor volume and weight inhibition of MLN8237 (20 mg/kg; p.o.) in vivo.
分子量
406.36
Formula
C18H17F3N6O2
CAS 号
1458630-17-5
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]. Huertas D, et al. Antitumor activity of a small-molecule inhibitor of the histone kinase Haspin. Oncogene. 2012 Mar 15;31(11):1408-18.
[2]. Han L, et al. Anti-Melanoma Activities of Haspin Inhibitor CHR-6494 Deployed as a Single Agent or in a Synergistic Combination with MEK Inhibitor. J Cancer. 2017 Aug 25;8(15):2933-2943.
[3]. Chen A, et al. CRISPR/Cas9 screening identifies a kinetochore-microtubule dependent mechanism for Aurora-A inhibitor resistance in breast cancer. Cancer Commun (Lond). 2021 Feb;41(2):121-139.
SHP2 protein degrader-1 is a potent allosteric inhibitor of SHP2. SHP2 protein degrader-1 induces SHP2 degradation and cell apoptosis. SHP2 protein degrader-1 has the potential for researching SHP2 related diseases[1].
IC50 & Target
SHP2[1]
体外研究 (In Vitro)
SHP2 protein degrader-1 (compound SP4) (0-200 μM; 24 hours) inhibits the growth of Hela cells, with IC50 of 5.77 and 4.30 nM, respectively, which are about 100 times higher than the activity of SHP099 (SHP2 inhibitor)[1]. SHP2 protein degrader-1 (compound SP4) (0-200 μM; 96 hours) induces 54.01% apoptotic death compared with 0.13% of the control at 100 nM[1]. SHP2 protein degrader-1 (compound SP4) (0-200 μM; 96 hours) induces cell cycle arrested at the G1 phase in Hela cells[1]. SHP2 protein degrader-1 (compound SP4) (0-200 μM; 96 hours) significantly inhibits the phosphorylation of JNK, Erk and p38[1]. SHP2 protein degrader-1 (compound SP4) (0-200 μM; 96 hours) inhibits RAS/MAPK signaling and cellular responses by a mechanism involving inhibition of SHP2 catalytic activity[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:
Hela cells
Concentration:
0-200 μM
Incubation Time:
24 hours
Result:
Strongly inhibited the growth of Hela cells, with IC50 of 5.77 and 4.30 nM, respectively, which were about 100 times higher than the activity of SHP099 (SHP2 inhibitor).
Apoptosis Analysis[1]
Cell Line:
Hela cells
Concentration:
0-100 μM
Incubation Time:
96 hours
Result:
Induced 54.01% apoptotic death compared with 0.13% of the control at 100 nM. While SHP099 at 1000 nM could induce 33.74% apoptotic death compared with 0.13% of the control.
Cell Cycle Analysis[1]
Cell Line:
Hela cells
Concentration:
0-100 μM
Incubation Time:
96 hours
Result:
Induced cell cycle arrested at the G1 phase in Hela cells.
Western Blot Analysis[1]
Cell Line:
Hela cells
Concentration:
0-100 μM
Incubation Time:
96 hours
Result:
Significantly inhibited the phosphorylation of JNK, Erk and p38.
分子量
908.83
Formula
C42H51Cl2N11O8
CAS 号
2624181-69-5
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]. Zheng M, et al. Novel PROTACs for degradation of SHP2 protein. Bioorg Chem. 2021;110:104788.
UPCDC-30245 is an allosteric p97 inhibitor with an IC50 of approximately 27 nM[1]. UPCDC-30245 inhibits the p97 mutant N660K similar to wild type (WT; IC50=300 nM) and shows 3-fold resistance for p97 mutant T688A[2]. UPCDC-30245 can be used in the research of cancer[1][2][3].
IC50 & Target[1][2]
allosteric p97
27 nM (IC50)
wild type p97
300 nM (IC50)
体外研究 (In Vitro)
UPCDC-30245 binds at the junction between the D1 dan D2 domains of p97[1]. UPCDC-30245 inhibits cell proliferation in HeLa, A549, BxPC-3, PRMI8226, MM1S, HCT116 cells, and appears more potent in HT29 cells[2]. UPCDC-30245 (0.01-100 μM) shows anti-proliferative effects on parental and CB-5083 resistant HCT116 cell lines that harbor a new p97 double mutation (D649A/T688A)[2]. UPCDC-30245 (4 μm; 2, 6, 10, 18, 24 hours; functional enrichment analysis) is not linked to pathways typically impacted by p97 inhibition, such as protein processing in the ER, UPR, and asparagine N-linked glycosylation[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
463.63
Formula
C28H38FN5
CAS 号
1883351-01-6
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]. Banerjee S, et al. 2.3 Å resolution cryo-EM structure of human p97 and mechanism of allosteric inhibition. Science. 2016 Feb 19;351(6275):871-5.
[2]. Wang F, et al. Allosteric p97 Inhibitors Can Overcome Resistance to ATP-Competitive p97 Inhibitors for Potential Anticancer Therapy. ChemMedChem. 2020 Apr 20;15(8):685-694.
[3]. Wang F, et al. Temporal proteomics reveal specific cell cycle oncoprotein downregulation by p97/VCP inhibition. Cell Chem Biol. 2021 Nov 23:S2451-9456(21)00482-7.
MS37452 is a potent inhibitor of CBX7 chromodomain binding to H3K27me3, with a Kd of 27.7 μM. MS37452 can derepress transcription of polycomb repressive complex target gene p16/CDKN2A by displacing CBX7 binding to the INK4A/ARF locus in prostate cancer cells[1].
IC50 & Target
CBX7[1]
体外研究 (In Vitro)
MS37452 (125-500 μM; 12 hours) significantly increases INK4A/ARF transcript levels up to 25% and 60% for 250 μM and 500 μM, respectively, as compared to the DMSO control[1]. MS37452 (250 μM; 2 hours) treats human PC3 prostate cancer cells for 2 hours reducing CBX7 occupancy across the INK4A/ARF locus[1]. MS37452 (200 µM; 5 days) combined with doxorubicin results in consistently decreased cell viability compared to DMSO treated and single drug treatment[2]. MS37452 (200 µM; 5 days), which is a CBX7 chromodomain inhibitor (CBX7i), in combination with doxorubicin is a novel therapeutic strategy[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.
RT-PCR[1]
Cell Line:
PC3 cells
Concentration:
125-500 μM
Incubation Time:
12 hours
Result:
Up-regulated INK4A/ARF expression up to 25% and 60% for 250 μM and 500 μM, respectively.
Identified several combinations that resulted in consistently decreased cell viability compared to DMSO treated and single drug treatment: SAHA/TMZ and MS37452/doxorubicin.
分子量
398.45
Formula
C22H26N2O5
CAS 号
423748-02-1
运输条件
Room temperature in continental US; may vary elsewhere.
Boc-NH-PEG11-OH is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs[1].
IC50 & Target
PEGs
体外研究 (In Vitro)
PROTACs contain two different ligands connected by a linker; one is a ligand for an E3 ubiquitin ligase and the other is for the target protein. PROTACs exploit the intracellular ubiquitin-proteasome system to selectively degrade target proteins[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
601.72
Formula
C27H55NO13
CAS 号
1556847-53-0
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]. An S, et al. Small-molecule PROTACs: An emerging and promising approach for the development of targeted therapy drugs. EBioMedicine. 2018 Oct;36:553-562
MIF-IN-5 (compound 1d) is a potent and reversible macrophage migration inhibitory factor (MIF) competitive inhibitor with an IC50 of 4.8 μM and a Ki value of 3.3 μM, respectively[1].
IC50 & Target
IC50: 4.8 μM (MIF)[1] Ki: 3.3 μM (MIF)[1]
分子量
351.33
Formula
C18H14FN5O2
CAS 号
2582755-31-3
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]. Xiao Z, Fokkens M, Chen D, et al. Structure-activity relationships for binding of 4-substituted triazole-phenols to macrophage migration inhibitory factor (MIF). Eur J Med Chem. 2020;186:111849.
GP-82996 (CINK4) is a pharmacological inhibitor of CDK4/6. GP-82996 has IC50s of 1.5, 5.6 and 25 μM for CDK4/cyclin D1, CDK6/cyclin D1 and Cdk5/p35, respectively. GP-82996 induces the apoptosis of cancer cells U2OS. GP-82996 can be used in the research of cancer[1][2].
IC50 & Target[1]
Cdk4/cyclin D1
1.5 μM (IC50)
CDK6/cyclinD1
5.6 μM (IC50)
CDK5/p35
25 μM (IC50)
CDK2/cyclinA
>50 μM (IC50)
CDK1/cyclinB
>100 μM (IC50)
CDK2/cyclin E
>50 μM (IC50)
CDK4/cyclin D2
>50 μM (IC50)
Cdk6/cyclin D2
>50 μM (IC50)
V-abl
>10 μM (IC50)
c-met
>10 μM (IC50)
IGF-1R
>10 μM (IC50)
Insulin-R
>10 μM (IC50)
体外研究 (In Vitro)
GP-82996 (5, 10 μM; 24 hours) induces G1 arrest and G0-G1/S ratio increase in U2OS (p16 negative) and MRC-5 (p16 positive) cells[1]. GP-82996 (5, 10 μM; 24 hours) reduces hyperphosphorylation of pRb, but has no changes in the levels of CDK4 in U2OS, MRC-5 cells[1]. GP-82996 (5, 10 μM; 48 hours) induces aooptosis in 83% of U2OS cells in concentration of 10μM[1]. GP-82996 (0.1-40 μM; 24,48, 72 hours) inhibits the cell proliferation of A549, H358, SKLU-1, H23, PC14 cells with IC50 values of 72 h are 4-7 μM[2]. GP-82996 (3, 5, 10 μM; 48 hours) induces G1 arrest in A549 and H23 cells[2]. GP-82996 ((1, 3, 5, 10 μM; 72 hours) enhances Paclitaxel sensitivity in KRAS mutation-bearing lung cancer cells (A549, SKLU-1, H23 cells) [2]. GP-82996 (10 μM; 72 hours) combined with Paclitaxel (3 nM; 72 hours) increases the apoptosis of A549 and H23 cells[2].
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)
GP-82996 (30 mg/kg, i.p. for 29 days) shows smaller final tumor volume compared with vehicle control in mouse xenograft models[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
19-21 g female BALB/c nu/nu mice xenograft model (HCT116 tumors volume=100 mm3)[1]
Dosage:
30 mg/kg
Administration:
i.p. every 12 hours for 29 days
Result:
Showed smaller final tumor volume compared with vehicle control in mouse xenograft models.
分子量
456.58
Formula
C27H32N6O
CAS 号
359886-84-3
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.
溶解性数据
In Vivo:
1.
5% DMSO, 0.05% Tween 80, and 95% physiologic saline
参考文献
[1]. Soni R, et al. Selective in vivo and in vitro effects of a small molecule inhibitor of cyclin-dependent kinase 4. J Natl Cancer Inst. 2001 Mar 21;93(6):436-46.
[2]. Zhang XH, et al. A CDK4/6 inhibitor enhances cytotoxicity of paclitaxel in lung adenocarcinoma cells harboring mutant KRAS as well as wild-type KRAS. Cancer Biol Ther. 2013;14(7):597-605.
CHR-6494 TFA is a potent inhibitor of haspin, with an IC50 of 2 nM. CHR-6494 TFA inhibits histone H3T3 phosphorylation. CHR-6494 TFA induces the apoptosis of cancer cells, including melanoma and breast cancer. CHR-6494 TFA can be used in the research of cancer[1][2][3].
IC50 & Target[1]
haspin
2 nM (IC50)
体外研究 (In Vitro)
CHR-6494 (TFA; 0-105 nM; 72 hours) dose-dependently inhibits the growth of cancer cells, such as HCT-116, HeLa, MDA-MB-231, and Wi-38 cells, with IC50s of 500 nM, 473 nM, 752 nM and 1059 nM, respectively[1]. CHR-6494 (TFA; 500 nM) produces a mitotic catastrophe with abnormal morphology of the mitotic spindle and centrosome amplification, and upregulates the spindle assembly checkpoint protein BUB1 and the marker of mitotic arrest cyclin B1[1]. CHR-6494 (TFA; 0, 0.5, 1.0 μM; 24 to 36 h) is an inhibitor of angiogenesis in the ex vivo chicken embryo aortic arch ring assay[1]. CHR-6494 (TFA) exhibits inhibitory activities against melanoma cell lines, including BRAFV600E mutants, NRAS mutants, and wild type cells, with IC50s ranging from 396 nM to 1229 nM[2]. CHR-6494 (TFA; 300 nM and 600 nM; 72 hours) induces apoptosis, increases caspase 3/7 activity by 3- and 6-fold, respectively in COLO-792 cells, and to 8.5- and 16-fold in RPMI-7951 melanoma cells[2]. CHR-6494 (TFA; 50, 200 nM; 1 week) enhances the antiproliferative effects of MLN8237 in MDA-MB-231, SKBR3 breast cancer cells[3]. CHR-6494 (TFA; 200 nM; 72 hours) enhances the apoptosis of MDA-MB-231 and SKBR3 cells when combined with MLN8237[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)
CHR-6494 (TFA; 50 mg/kg; i.p. in two cycles of five consecutive days for 15 days) inhibits the growth of tumor in nude mice bearing HCT-116 human colorectal cancer cells[1]. CHR-6494 (TFA; 20 mg/kg; intraperitoneal injection for 15 consecutive days) inhibits the tumor growth in nude mice bearing MDA-MB-231 xenograft tumors[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Male 4-5 weeks old athymic nu/nu mice harboring HCT-116 cells xenograft tumor with a tumor volume of 200 mm3[1]
Dosage:
50 mg/kg (diluted in a solution of 10% DMSO/20% 2-hydroxypropyl-b-cyclodextrin)
Administration:
i.p. in two cycles of five consecutive days for 15 days
Result:
Dose-dependent tumor growth inhibition was demonstrated. Did not change the body weight of mice.
20 mg/kg in a final formulation in 10% DMSO/20% 2‐hydroxypropyl‐β‐cyclodextrin
Administration:
i.p. for 15 consecutive days
Result:
Inhibited the tumor volume and weight compared with the control group in nude mice bearing MDA-MB-231 xenograft tumors. Enhanced the tumor volume and weight inhibition of MLN8237 (20 mg/kg; p.o.) in vivo.
分子量
406.36
Formula
C18H17F3N6O2
CAS 号
1458630-17-5
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]. Huertas D, et al. Antitumor activity of a small-molecule inhibitor of the histone kinase Haspin. Oncogene. 2012 Mar 15;31(11):1408-18.
[2]. Han L, et al. Anti-Melanoma Activities of Haspin Inhibitor CHR-6494 Deployed as a Single Agent or in a Synergistic Combination with MEK Inhibitor. J Cancer. 2017 Aug 25;8(15):2933-2943.
[3]. Chen A, et al. CRISPR/Cas9 screening identifies a kinetochore-microtubule dependent mechanism for Aurora-A inhibitor resistance in breast cancer. Cancer Commun (Lond). 2021 Feb;41(2):121-139.
Verrucarin J (Muconomycin B) is a metabolite of the Myrothecium fungus family. Verrucarin J generates reactive oxygen species (ROS) and induces apoptosis of cancer cell lines, such as A549, HCT 116 and SW-620 cells. Verrucarin J shows activities against Candida albicans and Mucor miehei. Verrucarin J inhibits arenavirus Junin (JUNV) yield with an IC50 of 1.2 ng/mL[1][2][3][4][5].
体外研究 (In Vitro)
Verrucarin J (0, 5, 10, 20, 50 nM; 24 hours) induces the apoptosis of A549 cells[1]. Verrucarin J (0, 1, 2, 5, 10, 20, 50 nM; 24, 48, 72 hours) significantly inhibits cell proliferation of A549 and H1793 cells with IC50 values of approximately 10 nM and 20 nM after 48 h of treatment, respectively[1]. Verrucarin J (0, 0.1, 0.2, 0.3, 0.4, 0.5 μM; 24 hours) has an IC50 of 300 nM for HCT 116 and SW-620 cell proliferation[2]. Verrucarin J (0, 10, 20 nM, 48 hours) inhibits cancer stem cell (CSC) self-renewal pathways Wnt1/β-catenin and Notch1 and down-regulates the expression of key CSC specific genes (ALDH1, LGR5, OCT4 and CD133) of A549 cells[1]. Verrucarin J (compound 2; 50 μg/disk) shows noteworthy activities against Candida albicans and Mucor miehei[3]. Verrucarin J reduces JUNV yield more than 2 log units and has a similar effect against the arenavirus Tacaribe[4]. Verrucarin J reduces the cell viability of Vero cells with a cytotoxic concentration 50% (CC50) of 8.2 ng/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)
Verrucarin J (0.5 mg/kg; i.p. for 4 weeks) suppresses AKT-induced tumor growth in a xenograft model[2]. Verrucarin J (0.1, 0.5, 2.0 mg/kg; i.p. for three weeks) is a highly potent anticancer drug and suppresses tumor growth and metastasis[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:
6-8 weeks old BALB/c athymic nude mice (nu/nu) with pCMV/HCT 116 and AKT/HCT 116 xenografts[2]
Dosage:
0.5 mg/kg body weight
Administration:
i.p. for 4 weeks
Result:
Reduced the expression of prosurvival markers pAKT, Notch1, p65, and Ki67 in all tumors.
Animal Model:
Female nude nu/nu (5 to 6 weeks old) mice with A2780 xenografts[5]
i.p. for three weeks after 10 days of injection of A2780 cells
Result:
Reduced tumor weight (32% lower compared to control), and reduced visible metastasis in 0.1 mg/kg. Showed a significant reduction in visible peritoneal tumors (61% lower compared to control group) and highly reduced visible metastasis in 0.5 mg/kg. Reduced ovarian tumor weight by 71% compared to vehicle in 0.5 mg/kg. In lethal dose 2 mg/kg, mice sick with a swollen belly, body fluid and subsequently died within 3 treatments.
分子量
484.54
Formula
C27H32O8
CAS 号
4643-58-7
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]. Udoh K, et al. Targeting of Lung Cancer Stem Cell Self-Renewal Pathway by a Small Molecule Verrucarin J. Stem Cell Rev Rep. 2019 Aug;15(4):601-611.
[2]. Pal D, et al. Suppression of Notch1 and AKT mediated epithelial to mesenchymal transition by Verrucarin J in metastatic colon cancer. Cell Death Dis. 2018 Jul 23;9(8):798.
[3]. Mondol MA, et al. Macrocyclic Trichothecenes from Myrothecium roridum Strain M10 with Motility Inhibitory and Zoosporicidal Activities against Phytophthora nicotianae. J Agric Food Chem. 2015 Oct 14;63(40):8777-86.
[4]. García CC, et al, Damonte EB. Evaluation of the antiviral activity against Junin virus of macrocyclic trichothecenes produced by the hypocrealean epibiont of Baccharis coridifolia. Planta Med. 2002 Mar;68(3):209-12.
[5]. Carter K, et al. Verrucarin J inhibits ovarian cancer and targets cancer stem cells. Oncotarget. 2017 Oct 6;8(54):92743-92756.
GSA-10 is a potent agonist of Smoothened (Smo) receptor with an EC50 of 1.2 μM. GSA-10 is a novel quinolinecarboxamide derivative. GSA-10 acts at Smo to promote the differentiation of multipotent mesenchymal progenitor cells into osteoblasts. GSA-10 mediates Hedgehog (Hh) signaling which may have researching interests in regenerative medicine for cancer disease[1][2].
IC50 & Target
Smoothened receptor[1]
分子量
450.53
Formula
C26H30N2O5
CAS 号
300833-95-8
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]. Manetti F, et al. Design, synthesis and biological characterization of a new class of osteogenic (1H)-quinolone derivatives. Eur J Med Chem. 2016;121:747-757.
[2]. Gorojankina T, et al. Discovery, molecular and pharmacological characterization of GSA-10, a novel small-molecule positive modulator of Smoothened [published correction appears in Mol Pharmacol. 2013 Aug;84(2):303]. Mol Pharmacol. 2013;83(5):1020-1029.
TNIK-IN-2 is a Traf2- and Nck-interacting protein kinase (TNIK) inhibitor, with an IC50 of 1.3337 μM[1].
IC50 & Target
IC50: 1.3337 μM (TNIK)[1]
体外研究 (In Vitro)
TNIK-IN-2 (compound 1) inhibits TNIK, with an IC50 of 31.26 μM in HCT116 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.
分子量
373.40
Formula
C22H19N3O3
CAS 号
2754265-76-2
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]. Li Y, et, al. Discovery of 3,4-Dihydrobenzo[ f][1,4]oxazepin-5(2 H)-one Derivatives as a New Class of Selective TNIK Inhibitors and Evaluation of Their Anti-Colorectal Cancer Effects. J Med Chem. 2022 Jan 5.
UPCDC-30245 is an allosteric p97 inhibitor with an IC50 of approximately 27 nM[1]. UPCDC-30245 inhibits the p97 mutant N660K similar to wild type (WT; IC50=300 nM) and shows 3-fold resistance for p97 mutant T688A[2]. UPCDC-30245 can be used in the research of cancer[1][2][3].
IC50 & Target[1][2]
allosteric p97
27 nM (IC50)
wild type p97
300 nM (IC50)
体外研究 (In Vitro)
UPCDC-30245 binds at the junction between the D1 dan D2 domains of p97[1]. UPCDC-30245 inhibits cell proliferation in HeLa, A549, BxPC-3, PRMI8226, MM1S, HCT116 cells, and appears more potent in HT29 cells[2]. UPCDC-30245 (0.01-100 μM) shows anti-proliferative effects on parental and CB-5083 resistant HCT116 cell lines that harbor a new p97 double mutation (D649A/T688A)[2]. UPCDC-30245 (4 μm; 2, 6, 10, 18, 24 hours; functional enrichment analysis) is not linked to pathways typically impacted by p97 inhibition, such as protein processing in the ER, UPR, and asparagine N-linked glycosylation[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
463.63
Formula
C28H38FN5
CAS 号
1883351-01-6
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]. Banerjee S, et al. 2.3 Å resolution cryo-EM structure of human p97 and mechanism of allosteric inhibition. Science. 2016 Feb 19;351(6275):871-5.
[2]. Wang F, et al. Allosteric p97 Inhibitors Can Overcome Resistance to ATP-Competitive p97 Inhibitors for Potential Anticancer Therapy. ChemMedChem. 2020 Apr 20;15(8):685-694.
[3]. Wang F, et al. Temporal proteomics reveal specific cell cycle oncoprotein downregulation by p97/VCP inhibition. Cell Chem Biol. 2021 Nov 23:S2451-9456(21)00482-7.
MRT-83 (hydrochloride) is the potent antagonist of Smoothened (Smo) receptor. MRT-83 (hydrochloride) inhibits the Hedgehog (Hh) signaling pathway and BODIPY-cyclopamine binding to human Smo. MRT-83 (hydrochloride) has the potential for researching cancer disease[1].
IC50 & Target
Smo[1]
体外研究 (In Vitro)
MRT-83 (hydrochloride) (compound 86) has IC50s of 15 and 11 nM respectively in Shh-light2 and C3H10T1/2 cells in the biological activity assay[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
575.05
Formula
C31H31ClN4O5
CAS 号
1359944-60-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Solinas A, et al. Acylthiourea, acylurea, and acylguanidine derivatives with potent hedgehog inhibiting activity. J Med Chem. 2012;55(4):1559-1571.
Ajoene, a garlic-derived compound, is an antithrombotic and antifungal agent. Ajoene inhibits proliferation and induces apoptosis of human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-I. Anticancer activities[1][2].
体外研究 (In Vitro)
Ajoene shows cytotoxicity with IC50s in the 7-41 uM range for B16/BL6, HT-29, A549, MDA-MB231, PANC-1, and SKBR-3 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)
Ajoene (25 μg/g body weight of Ajoene in 100 mL Intralipid; i.p.; every other day from the day of inoculation up to day 28) inhibits both primary tumor growth[1]. Ajoene (25, 15 or 5 μg/g body weight of Ajoene in 100 μL Intralipid; i.p; every other day over 4 weeks) inhibits strongly metastasis to lung in the B16/BL6 melanoma tumor model in C57BL/6 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.
分子量
234.40
Formula
C9H14OS3
CAS 号
92285-01-3
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]. Taylor P, et al. Ajoene inhibits both primary tumor growth and metastasis of B16/BL6 melanoma cells in C57BL/6 mice. Cancer Lett. 2006;239(2):298-304.
[2]. Ahmed N, et al. Ajoene, a garlic-derived natural compound, enhances chemotherapy-induced apoptosis in human myeloid leukaemia CD34-positive resistant cells. Anticancer Res. 2001;21(5):3519-3523.
GP-82996 (CINK4) is a pharmacological inhibitor of CDK4/6. GP-82996 has IC50s of 1.5, 5.6 and 25 μM for CDK4/cyclin D1, CDK6/cyclin D1 and Cdk5/p35, respectively. GP-82996 induces the apoptosis of cancer cells U2OS. GP-82996 can be used in the research of cancer[1][2].
IC50 & Target[1]
Cdk4/cyclin D1
1.5 μM (IC50)
CDK6/cyclinD1
5.6 μM (IC50)
CDK5/p35
25 μM (IC50)
CDK2/cyclinA
>50 μM (IC50)
CDK1/cyclinB
>100 μM (IC50)
CDK2/cyclin E
>50 μM (IC50)
CDK4/cyclin D2
>50 μM (IC50)
Cdk6/cyclin D2
>50 μM (IC50)
V-abl
>10 μM (IC50)
c-met
>10 μM (IC50)
IGF-1R
>10 μM (IC50)
Insulin-R
>10 μM (IC50)
体外研究 (In Vitro)
GP-82996 (5, 10 μM; 24 hours) induces G1 arrest and G0-G1/S ratio increase in U2OS (p16 negative) and MRC-5 (p16 positive) cells[1]. GP-82996 (5, 10 μM; 24 hours) reduces hyperphosphorylation of pRb, but has no changes in the levels of CDK4 in U2OS, MRC-5 cells[1]. GP-82996 (5, 10 μM; 48 hours) induces aooptosis in 83% of U2OS cells in concentration of 10μM[1]. GP-82996 (0.1-40 μM; 24,48, 72 hours) inhibits the cell proliferation of A549, H358, SKLU-1, H23, PC14 cells with IC50 values of 72 h are 4-7 μM[2]. GP-82996 (3, 5, 10 μM; 48 hours) induces G1 arrest in A549 and H23 cells[2]. GP-82996 ((1, 3, 5, 10 μM; 72 hours) enhances Paclitaxel sensitivity in KRAS mutation-bearing lung cancer cells (A549, SKLU-1, H23 cells) [2]. GP-82996 (10 μM; 72 hours) combined with Paclitaxel (3 nM; 72 hours) increases the apoptosis of A549 and H23 cells[2].
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)
GP-82996 (30 mg/kg, i.p. for 29 days) shows smaller final tumor volume compared with vehicle control in mouse xenograft models[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
19-21 g female BALB/c nu/nu mice xenograft model (HCT116 tumors volume=100 mm3)[1]
Dosage:
30 mg/kg
Administration:
i.p. every 12 hours for 29 days
Result:
Showed smaller final tumor volume compared with vehicle control in mouse xenograft models.
分子量
456.58
Formula
C27H32N6O
CAS 号
359886-84-3
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.
溶解性数据
In Vivo:
1.
5% DMSO, 0.05% Tween 80, and 95% physiologic saline
参考文献
[1]. Soni R, et al. Selective in vivo and in vitro effects of a small molecule inhibitor of cyclin-dependent kinase 4. J Natl Cancer Inst. 2001 Mar 21;93(6):436-46.
[2]. Zhang XH, et al. A CDK4/6 inhibitor enhances cytotoxicity of paclitaxel in lung adenocarcinoma cells harboring mutant KRAS as well as wild-type KRAS. Cancer Biol Ther. 2013;14(7):597-605.
Palmitic acid-13C sodium is the 13C-labeled Palmitic acid. Palmitic acid is a long-chain saturated fatty acid commonly found in both animals and plants. Palmitic acid can induce the expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in in mouse granulosa cells[1][2].
分子量
279.40
Formula
C1513CH31NaO2
CAS 号
201612-54-6
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Harada H, et al. Antitumor activity of palmitic acid found as a selective cytotoxic substance in a marine red alga. Anticancer Res. 2002 Sep-Oct;22(5):2587-90.
MIF-IN-6 (compound 2d) is a potent macrophage migration inhibitory factor (MIF) inhibitor with an IC50 of 1.4 μM and a Ki value of 0.96 μM, respectively. MIF-IN-6 attenuates MIF-induced ERK phosphorylation and inhibits proliferation of A549 cells[1].
IC50 & Target
IC50: 1.4 μM (MIF)[1] Ki: 0.96 μM (MIF)[1]
分子量
385.78
Formula
C18H13ClFN5O2
CAS 号
2582758-61-8
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]. Xiao Z, Fokkens M, Chen D, et al. Structure-activity relationships for binding of 4-substituted triazole-phenols to macrophage migration inhibitory factor (MIF). Eur J Med Chem. 2020;186:111849.
Naphthofluorescein inhibits the interaction between HIF-1 and Mint3. Naphthofluorescein suppresses Mint3-dependent HIF-1 activity and glycolysis in cancer cells and macrophages without cytotoxicity in vitro and adverse effect in vivo[1]. Naphthofluorescein is also a fluorescent pH-sensitive probe that can be used for functional Cerenkov imaging[2].
IC50 & Target
HIF-1[1]
体外研究 (In Vitro)
Naphthofluorescein (compound 19) (0-10 μM; 24 hours) suppresses the HIF-1 reporter activity 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.
Cell Viability Assay[1]
Cell Line:
HT1080 cells
Concentration:
0-10 μM
Incubation Time:
24 hours
Result:
Significantly suppressed the HIF-1 reporter activity in a concentration-dependent manner.
体内研究 (In Vivo)
Naphthofluorescein (compound 19) (100 mg/kg; i.p.; once daily for 5 consecutive days followed by 2 days off for 2 weeks)does not show weight loss or apparent histological abnormalities in the lung, liver, and kidney, or cause cause severe adverse effects for at least 2 weeks in mice[1]. Naphthofluorescein (compound 19) (100 mg/kg; i.p.; once daily for 5 consecutive days followed by 2 days off for 2 weeks) strikingly suppresses the tumour growth of subcutaneously injected E0771 cells and significantly attenuates tumour growth of MDA-MB-231 and AsPC-1 cells in immunodeficient mice. In turn, naphthofluorescein does not attenuate tumour growth of FIH-1-depleted MDA-MB-231 cells[1]. Naphthofluorescein (compound 19) (100 mg/kg; i.p.; once daily for 5 consecutive days followed by 2 days off for 2 weeks) suppresses tumour growth in human cancer cells in an FIH-1-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.
Animal Model:
Male C57BL/6J mice (8 weeks)[1]
Dosage:
100 mg/kg
Administration:
i.p.; once daily for 5 consecutive days followed by 2 days off for 2 weeks
Result:
Neither showed weight loss or apparent histological abnormalities in the lung, liver, and kidney, or caused cause severe adverse effects for at least 2 weeks in mice.
Animal Model:
Female C57BL/6J mice (E0771) and BALB/c nude mice (HT1080, MDA-MB-231, and AsPC-1) (6 weeks)[1]
Dosage:
100 mg/kg
Administration:
i.p.; once daily for 5 consecutive days followed by 2 days off for 2 weeks
Result:
Strikingly suppressed the tumour growth of subcutaneously injected E0771 cells and significantly attenuated tumour growth of MDA-MB-231 and AsPC-1 cells in immunodeficient mice. In turn, naphthofluorescein did not attenuate tumour growth of FIH-1-depleted MDA-MB-231 cells.
分子量
432.42
Formula
C28H16O5
CAS 号
61419-02-1
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]. Sakamoto T, et al. Pharmacological inhibition of Mint3 attenuates tumour growth, metastasis, and endotoxic shock. Commun Biol. 2021;4(1):1165. Published 2021 Oct 7.
[2]. Arroyo AD, et al. Development of fluorinated naphthofluoresceins for Cerenkov imaging. J Fluor Chem. 2019;225:27-34.
