aspc-1 cells

Almorexant (ACT 078573) is a potent and competitive dual orexin 1 receptor (OX1)/orexin 2 receptor (OX2) antagonist with Ki values of 1.3 and 0.17 nM for OX1 and OX2, respectively.

Almorexant hydrochloride (ACT 078573 hydrochloride) is an orally active dual orexin receptor antagonist that blocks the intracellular Ca2+ signaling pathway and, to a certain extent, blocks the excitatory effects of methamphetamine. Almorexant hydrochloride Induces apoptosis and can be used to study sleep disorders.

RMC-9805 is a novel, mutant-selective, covalent and oral KRASG12D (ON) inhibitor. A stable and high affinity triple complex is formed between RMC-9805, KRASG12D, and cyclophilin A, which inhibits signal transduction downstream of KRASG12D (ON) by disrupting its interaction with downstream effectors. RMC-9805 can induce cell apoptosis and promote tumor regression in preclinical KRASG12D tumor models. With rich experience in compound synthesis, we can provide fast customized synthesis services for this product according to your research needs.

KRAS inhibitor-27 (Compound 15h) is a KRAS inhibitor that effectively targets KRAS G12D/G12V mutated cells (AsPC-1 and SW620) and wild-type KRAS cells (HT-29), with IC50 values of 378 nM, 0.6 nM, and 3230 nM, respectively. It reduces ERK phosphorylation, with IC50 values of 0.6 nM and 1 nM in AsPC-1 and SW620 cells, respectively, and decreases DUSP4 expression, thereby inhibiting the MAPK signaling pathway.

5-HT1AR/5-HT6R ligand-1 (Compound PP13) functions as a ligand for the 5-HT receptor, demonstrating high affinity for 5-HT1AR, 5-HT6R, and 5-HT7R with Ki values of 19, 69, and 198 nM, respectively. In HEK293 cells, it inhibits cAMP production with EC50 values of 1535, 488, and 53 nM for these receptors. Additionally, 5-HT1AR/5-HT6R ligand-1 exhibits antiproliferative effects on several cancer cell lines, including 1321N1, U87MG, MCF7, and AsPC-1, with IC50 values of 9.6, 13.6, 19.3, and 14.6 μM, respectively. The compound also shows antagonistic activity towards the dopamine receptor D2R, with a Ki of 1903 nM.

KRASG12D-IN-3-d3 is the deuterium labeled KRASG12D-IN-3. KRASG12D-IN-3 (compound Z1084) is a KRASG12D inhibitor with oral bioactivity that can effectively inhibit the growth of tumor cells AGS and AsPC-1, with IC50 values of 0.38 nM and 1.23 nM, respectively.

KRASG12D-IN-3 (compound Z1084) is a KRASG12D inhibitor with oral bioactivity that can effectively inhibit the growth of tumor cells AGS and AsPC-1, with IC50 values of 0.38 nM and 1.23 nM, respectively.

CDK2/FLT4/PDGFRA-IN-1 (Compound 4a) is a potent inhibitor of CDK2/cyclin A, FLT4 (VEGFR3), and PDGFRA, with IC50 values of 1.672, 0.554, and 0.629 μM respectively. This compound demonstrates significant antiproliferative effects on cancer cells, including lung cancer EBC-1, pancreatic ductal adenocarcinoma AsPC-1, and colorectal cancer HT-29 cells. Additionally, CDK2/FLT4/PDGFRA-IN-1 can induce apoptosis in these cancer cells.

pan-KRAS-IN-8 (Compound 38) is an inhibitor of the human tumor mutated gene KRAS. It effectively suppresses the proliferation of KRAS mutant cells AsPC-1 (G12D mutant) and SW480 (G12V mutant), with IC50 values of 0.07 nM and 0.18 nM, respectively.

Pan-KRAS-IN-10 (Compound 58) acts as an inhibitor of the human tumor mutant gene KRAS. It suppresses the proliferation of KRAS mutant cells, specifically AsPC-1 (G12D mutant) and SW480 (G12V mutant), with IC50 values of 0.7 and 0.24 nM, respectively.

pan-KRAS-IN-7 (Compound 25) is an inhibitor of the human tumorigenic mutant gene KRAS. It effectively suppresses the proliferation of KRAS mutant cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with an IC50 of 0.35 nM and 0.51 nM, respectively.

Pan-KRAS-IN-8 (Compound 52) is an inhibitor of the human tumor mutant gene KRAS. It suppresses the proliferation of KRAS mutant cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with IC50 values of 0.24 nM and 0.30 nM, respectively.

KRASG12D-IN-5 (Compound 241) is an orally active KRAS(G12D) inhibitor with an IC50 of 11 nM. It demonstrates potent anticancer activity without significant cytotoxicity to BxPC-3 cells (wild-type), KRAS-mutant AsPC-1 cells (G12D), and MIAPaCa-2 cells (G12C), with CC50 values of 10.37, 0.76, and 0.3 μM, respectively. KRASG12D-IN-5 is applicable in cancer studies, including lung, pancreatic, and colorectal cancers.

CH091138 is a potent and selective KRASG12D PROTAC degrader, exhibiting a DC50 value of 148.3 nM in HeLa cells and 469.8 nM in AsPC-1 cells. It selectively targets both exogenous and endogenous KRASG12D through the VHL-mediated ubiquitin-proteasome system, without affecting KRASWT or other KRAS mutants (G12C/G12S/G12V). CH091138 demonstrates significant antitumor activity by inducing apoptosis (apoptosis) in tumor cells and is applicable for research in pancreatic and colon cancers.

CIDD-8633 is a potent inhibitor of DDR2 with an IC50 of 6.105 μM. It significantly suppresses the proliferation of MIA-PaCa-2 and AsPC-1 cells, with IC25 values of 4.0 and 5.5 μM, respectively. Additionally, CIDD-8633 hinders cell migration, arrests the cell cycle, induces apoptosis (apoptosis), and substantially reduces the growth of pancreatic ductal adenocarcinoma (PDAC) tumors. This compound is applicable in pancreatic cancer research, including studies on PDAC.

KRASG12D-IN-7 is a selective inhibitor of KRASG12D. It exhibits strong binding affinity to KRASG12D in both GDP-bound and GTP-bound states, with Kd values of 1.12 nM and 1.86 nM, respectively. This compound inhibits the proliferation of KRASG12D-bearing AsPC-1 cells with an IC50 of 10 nM and disrupts MAPK signaling. In AsPC-1 cells, KRASG12D-IN-7 induces G0/G1 phase arrest and apoptosis (apoptosis), and significantly suppresses colony formation. The inhibitor is applicable for research on cancers with KRASG12D mutations, particularly pancreatic ductal adenocarcinoma (PDAC).

Aspulvinone O is a fungal metabolite that has been found in P. variotti and has antioxidant and anticancer activities.1,2 It scavenges 2,2-diphenyl-1-picrylhydrazyl radicals in a cell-free assay (IC50 = 11.6 μM).1 Aspulvinone O inhibits aspartate transaminase 1 (GOT1; Kd = 3.32 μM) and is cytotoxic to PANC-1, AsPC-1, and SW1990 pancreatic cancer cells (IC50s = 20.54-26.8 μM).2 It reduces the oxygen consumption rate (OCR) and induces apoptosis in SW1990 cells. Aspulvinone O (2.5 and 5 mg/kg) reduces tumor growth in an SW1990 mouse xenograft model. |1. Zhang, P., Li, X.-M., Wang, J.-N., et al. New butenolide derivatives from the marine-derived fungus Paecilomyces variotii with DPPH radical scavenging activity. Phytochem. Lett. 11, 85-88 (2015).|2. Sun, W., Luan, S., Qi, C., et al. Aspulvinone O, a natural inhibitor of GOT1 suppresses pancreatic ductal adenocarcinoma cells growth by interfering glutamine metabolism. Cell Commun. Signal. 17(1), 111 (2019).

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

GM 1489 is a broad-spectrum inhibitor of matrix metalloproteinases (MMPs) with Ki values of 0.002, 0.1, 0.5, 0.2, and 20 μM for MMP-1, MMP-8, MMP-2, MMP-9, and MMP-3, respectively. It reduces 5-aza-2'-deoxycytidine-induced increases in MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, and MMP-14 expression as well as cell invasion in AsPC-1, BxPC-3, Hs766T, MiaPaCa2, and PANC-1 cancer cells. Topical administration of GM 1489 (100 μg) inhibits increases in ear thickness and epidermal hyperplasia induced by phorbol 12-myristate 13-acetate and phorbol dibutyrate (PdiBu) in mice.

MET/PDGFRA-IN-2 (compound 8h) is an inhibitor of MET and PDGFRA proteins that promotes apoptosis and impedes proliferation of MET-positive cells with IC50 values of 9.7, 6.1, 12.0, 11.5, 8.6, and 34.4 μM for AsPc-1, EBC-1, MKN-45, Mia-Paca-2, HT-29, and K562 cells, respectively [1].