pancreatic ductal adenocarcinoma (pdac)

FAK-IN-22 (Compound 26) is an inhibitor of FAK, JAK3, and Aurora B, with IC50 values of 50.94 nM, 9.99 nM, and 0.49 nM, respectively, effectively suppressing tumorigenesis and metastasis in pancreatic ductal adenocarcinoma (PDAC). It inhibits proliferation in PANC-1 cells with an IC50 of 0.15 μM. FAK-IN-22 induces apoptosis and G2/M phase arrest in PANC-1 cells by inhibiting the FAK/PI3K/Akt signaling pathway.

ROCK/HDAC-IN-2 (Compound C-9) is a dual inhibitor of ROCK/HDAC, characterized by IC50 values of 0.185 µM for HDAC6, 0.8 µM for ROCK1, and 0.7 µM for ROCK2. It effectively induces apoptosis and mitochondrial membrane potential alterations in cancer cells and demonstrates notable antitumor activity, making it useful for research in pancreatic ductal adenocarcinoma (PDAC) and triple-negative breast cancer (TNBC).

LIB3S0280 is a potent inhibitor of TBK1, with an IC50 of 493.9 nM. It suppresses TBK1 downstream signaling by reducing the phosphorylation of IκBα and AKT. LIB3S0280 causes G2/M phase arrest and induces apoptosis in pancreatic cancer cells. Notably, it exhibits significant inhibitory effects on pancreatic cancer cell lines with high TBK1 expression, with a 96-hour IC50 value ranging from 6.64-10.98 μM. LIB3S0280 shows potential for research in pancreatic ductal adenocarcinoma (PDAC).

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).

5-Methyl cromolyn (C5OH) disodium is a cromolyn analog that acts as an S100P inhibitor. It prevents the interaction between S100P and its receptor RAGE, hinders NF-κB activity and cell proliferation, and enhances apoptosis induced by Gemcitabine. In murine models with PDAC, 5-Methyl cromolyn disodium reduces tumor growth and metastasis, thereby extending survival. This compound is suitable for pancreatic cancer research, including studies on pancreatic ductal adenocarcinoma (PDAC).

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.

MMRi62 (7-[(2,3-dichlorophenyl)-(pyridin-2-ylamino)methyl]quinolin-8-ol), a ferroptosis inducer targeting MDM2-MDM4 (negative regulators of tumor suppressor p53). MMRi62 shows a P53-independent pro-apoptotic activity against pancreatic ductal adenocarcinoma (PDAC) cells and induce autophagy. MMRi62 inducesferroptosis, resulting in a increase of reactive oxygen and lysosomal degradation of ferritin heavy chain (FTH1). MMRi62 also leads to proteasomal degradation of mutant p53, also inhibits orthotopic xenograft PDAC mouse model in vivo with high frequency mutation characteristics of KRAS and TP53.12.

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.

XP-524 is a potent inhibitor of BET and EP300. XP-524 has significant tumouricidal effects in vivo, preventing KRAS-induced tumour transformation in vivo and prolonging survival in two aggressive PDAC transgenic mouse models. XP-524 also enhances the expression of its own peptide and recruitment of tumour cells to cytotoxic T lymphocytes. XP-524 has shown potential for research in pancreatic ductal adenocarcinoma (PDAC).

SIRT6-IN-3 (compound 8a), a selective SIRT6 inhibitor (IC50 = 7.49 μM), impedes the proliferation of pancreatic ductal adenocarcinoma (PDAC) cells and prompts apoptosis. It enhances the responsiveness of cancer cells to gemcitabine by obstructing the DNA damage repair pathway, thus serving as a valuable tool in pancreatic cancer research [1].

GOT1 inhibitor-1 (GOT1 inhibitor 2c) is a novel, potent and non-covalent inhibitor of glutamate oxaloacetate transaminase 1 (GOT1) with an IC50 of 8.2 uM.

EBET-1055 is a degrader of bromodomain and extra-terminal (BET) proteins, consisting of a BET inhibitor (EBET-590), an E3 ubiquitin ligase ligand, and connectors. It effectively inhibits the growth of pancreatic ductal adenocarcinoma (PDAC) and also modulates cancer-associated fibroblast (CAF) activity, enhancing all reporter gene activities in organoid co-cultures [1].

Argyrin F is a cyclopeptide with antitumor properties. It inhibits cell proliferation, migration, invasion, and colony formation by partially inducing apoptosis (apoptosis) and epithelial-mesenchymal transition (EMT). Argyrin F stabilizes p27kip, upregulates p21waf1/cip1, and reduces COX2. Argyrin F is applicable for research in pancreatic ductal adenocarcinoma (PDAC).

Unlabeled FXX489 (NNS309) is a ligand that targets fibroblast activation protein (FAP). It can be labeled with 68Ga and 177Lu, exhibiting anti-cancer properties. Unlabeled FXX489 is utilized in the study of pancreatic ductal adenocarcinoma (PDAC), non-small cell lung cancer (NSCLC), breast cancer (BC), and colorectal cancer (CRC).

(R,R)-VRT-534 is the enantiomer of VRT-534. EBET-1055 is a bromodomain and extra-terminal (BET) PROTAC degrader. It effectively inhibits the growth of pancreatic ductal adenocarcinoma (PDAC). Additionally, EBET-1055 modulates cancer-associated fibroblast (CAF) activity, increasing the activity of all reporter genes in organoid co-cultures.