breast cancer cell death

SI-2 hydrochloride (EPH 116 hydrochloride) is a highly promising inhibitor of SRC-3 SMI: SRC-3 (PPI)(IC50 values of 3-20 nM for breast cancer cell death), with acceptable oral availability.

SI-2 is an inhibitor (SMI) of steroid receptor coactivator-3 (SRC-3 or AIB1). SI-2 can selectively reduce the transcriptional activities and the protein concentrations of SRC-3 in cells, and selectively induce breast cancer cell death with IC50 values in the low nanomolar range (3-20 nM), but not affect normal cell viability.

HJ-PI01 (HJ-PI01) is a Pim-2 inhibitor. HJ-PI01 (HJ-PI01) induces apoptosis and autophagic cell death in triple-negative human breast cancer.

OUP-186 is a high affinity and human/rat species-selective antagonist of histamine H3 receptor. OUP-186 suppressed the proliferation of breast cancer cells. The IC50 values at 48 hours for OUP-186 was approximately 50 μM. OUP-186 potently induced cell dea

Larotaxel (XRP9881) is a taxane analogue with anticancer activity that promotes tubulin assembly and stabilizes microtubules, inducing apoptosis. It crosses the blood-brain barrier and has a higher affinity for Docetaxel than P-glycoprotein 1, making it useful for studying breast and bladder cancer.

ROCK/HDAC-IN-1 (Compound 10h) serves as an orally effective inhibitor of ROCK/HDAC. This compound suppresses ROCK1/2 (IC50: 254.9 nM, 58.18 nM) and HDAC1/2/3/6/8 (IC50: 9.09, 8.03, 6.26, 0.41, 7.69 nM). It stimulates the activation of DAMPs, notably calreticulin (CRT) exposure and HMGB1 release, suggesting its potential as an inducer of immunogenic cell death (ICD). ROCK/HDAC-IN-1 exhibits antiproliferative effects against breast cancer cells (IC50: 0.37 μM for MDA-MB-231 cells), inhibits tumor growth, activates T cells, and shows no significant toxicity.

LXG6403 is a powerful dual-thiazole LOX cell activity inhibitor with an IC50 of 1.3 μM. It exhibits anticancer properties by restructuring the extracellular matrix, enhancing the penetration of chemotherapeutic drugs, inducing reactive oxygen species (ROS) production, and promoting cell death mediated by DNA damage, thereby overcoming chemotherapy resistance in triple-negative breast cancer.

ERK1/2 inhibitor 10 (Compound 36c) is a potent inhibitor of ERK1 and ERK2, with IC50 values of 0.11 nM and 0.08 nM, respectively. It effectively hinders the phosphorylation of downstream substrates p90RSK and c-Myc. Additionally, ERK1/2 inhibitor 10 induces apoptosis and incomplete autophagy-related cell death. This compound demonstrates significant antitumor efficacy in models of triple-negative breast cancer and colorectal cancer harboring BRAF and RAS mutations.

F3-PEG8-RiboTAC is a RiboTAC compound that specifically degrades the mRNA of the oncogene LGALS1. This compound can induce apoptosis (cell death) in tumor cells and inhibit their invasion. F3-PEG8-RiboTAC exhibits antitumor activity and is applicable in research on leukemia and triple-negative breast cancer. (RNase L ligand; RNA binder; Linker)

TNI-97 is a selective, orally active HDAC6 inhibitor with an IC50 value of 0.2 nM. It significantly suppresses the growth and colony-forming abilities of the triple-negative breast cancer (TNBC) cell line MDA-MB-453. In these cells, TNI-97 induces widespread cell death, including apoptosis, necroptosis, and pyroptosis. Additionally, TNI-97 demonstrates antitumor activity in mouse models bearing MDA-MB-453 xenograft tumors or syngeneic mouse-derived TNBC cell allograft tumors. TNI-97 is useful for researching triple-negative breast cancer.

Ferroptosisinducer-8 is a ferroptosis (iron-dependent cell death) inducer with high selectivity against other cell death pathways. It induces ferroptosis by affecting ACSL4, GPX4, and FTH1, disrupting intracellular iron homeostasis and the GSH/GPX4 antioxidant defense system, leading to the accumulation of lipid peroxides. Ferroptosisinducer-8 also stimulates ROS production and can inhibit tumor growth, making it useful for research in triple-negative breast cancer (TNBC).

Apoptosis inducer41 is an apoptosis-inducing agent that prompts cell death through the mitochondrial pathway. It exhibits significant inhibitory effects on MCF-7 cells, with an IC50 of 6.2 μM. Apoptosis inducer41 notably arrests MCF-7 cells in the G2/M phase, increases the accumulation of reactive oxygen species (ROS), and induces mitochondrial membrane potential depolarization. This compound is applicable in breast cancer research.

Chloroxoquinoline is an anticancer agent that disrupts the DNA template of cancer cells, leading to DNA breaks and cell death. It inhibits cell invasion by downregulating the Rho/Rho kinase signaling pathway. In tumor-bearing mouse models, Chloroxoquinoline enhances the radiosensitivity of Lewis lung carcinoma cells and xenograft tumors. However, its long-term efficacy is reduced in rat models due to self-induction of CYP1A and CYP3A. Chloroxoquinoline exhibits broad-spectrum anticancer activity against non-small cell lung cancer (NSCLC), breast cancer, and gastric cancer.

Apoptosis inducer46 is an apoptosis (apoptosis) inducer that exhibits potent and selective growth inhibitory effects on metastatic triple-negative breast cancer (TNBC) cells. It induces G2/M phase cell cycle arrest and apoptosis (apoptosis) cell death in MDA-MB-231 cells and blocks the nuclear translocation of NF-κB. Apoptosis inducer46 is useful for TNBC research.

Kahalalide F is a novel marine-derived antitumor agent known for inhibiting DNA synthesis. It exhibits cytotoxicity that is not correlated with the expression levels of the multidrug resistance gene MDR1 or the tyrosine kinase HER2/NEU, and is only slightly related to the expression of the anti-apoptotic protein BCL-2. Kahalalide F hinders the PI3K-Akt signaling pathway by depleting ErbB3. Its effects are rapidly activated with short pulse treatments. The compound primarily induces cell death through oncosis (cellular swelling) in tumor cells. Kahalalide F can be utilized in studies of prostate cancer, breast cancer, vulvar cancer, and non-small cell lung cancer.

Sino-C is a Sinomenine derivative with anticancer properties. It disrupts cholesterol homeostasis by upregulating crucial genes such as SREBF2 and HMGCS1, leading to intracellular cholesterol accumulation and lipid droplet formation. The metabolic disturbance induced by Sino-C further triggers lipid peroxidation and endoplasmic reticulum (ER) stress, initiating a unique mixed form of cell death that includes both apoptotic (cleaved PARP) and necrotic-like features. Sino-C is applicable in studies of colorectal cancer, lung cancer, and breast cancer.

STAT3-IN-51 is a STAT3 inhibitor that binds directly to the SH2 domain of STAT3. This compound induces apoptosis, ferroptosis, and immunogenic cell death (ICD), enhancing antitumor immunity. It suppresses STAT3 activation (phosphorylation, p-STAT3) and its downstream signaling, while prompting reactive oxygen species (ROS) generation, decreasing Bcl-2 expression, disrupting mitochondrial functions, inhibiting GPX4 activity, and promoting lipid peroxidation. STAT3-IN-51 is applicable in research on colorectal cancer, breast adenocarcinoma, non-small cell lung cancer (NSCLC), and cisplatin-resistant lung adenocarcinoma.

Anti-TNBC agent-13 is a NO donor-Aurovertin B conjugate that can induce ferroptosis. It inhibits GPX4 activity, leading to cell death in triple-negative breast cancer (TNBC) cells. Anti-TNBC agent-13 is useful for research in triple-negative breast cancer.

PARP1/EZH2-IN-1 is a selective dual inhibitor targeting both PARP1 and EZH2. It exhibits IC50 values of 28 nM for PARP1, 414 nM for PARP2, and 74 nM for EZH2. This compound inhibits the proliferation and migration of TNBC cells (triple-negative breast cancer cells). It can induce PANoptosis, a form of cell death that includes apoptosis, pyroptosis, and necroptosis, elevate reactive oxygen species (ROS) levels, and activate associated inflammatory pathways. PARP1/EZH2-IN-1 is applicable in research related to triple-negative breast cancer.

Tingenin B is a potent anticancer agent due to its cytotoxic activity on cancer stem cells of breast cancer in vitro. Tingenin b was cytotoxic against MCF-7s (IC50: 2.38 μM for 48 h) by inducing apoptosis. Endoplasmic reticulum stress was also found to be

Collismycin A is a bacterial metabolite from *Streptomyces* with antibacterial, antiproliferative, and neuroprotective properties. It exhibits activity against various bacteria (MICs = 6.25-100 μg/ml) and fungi (MICs = 12.5-100 μg/ml). It inhibits proliferation of A549 lung, HCT116 colon, and HeLa cervical cancer cells (IC50s = 0.3, 0.6, and 0.3 μM, respectively) and NIH373 fibroblasts (IC50 = 56.6 μM) but not MDA-MD-231 breast cancer cells (IC50 > 100 μM). Collismycin A forms a complex with Fe(II) and Fe(III) in a 2:1 ratio, with iron ions inhibiting its antiproliferative effect on HeLa cells, an effect not observed with zinc, manganese, copper, or magnesium ions. Additionally, Collismycin A (1 μM) reduces apoptosis in zebrafish larvae brain regions by 44% in a model of neuronal cell death induced by all-trans retinoic acid.

DMBA (7,12-Dimethylbenz[a]anthracene) is a carcinogenic polycyclic aromatic hydrocarbon (PAH) that can be used to induce animal models of leukemia, liver cancer, breast cancer, skin cancer, and lung cancer. It is also capable of inducing programmed cell death (apoptosis) in A20.1 murine B-cell lymphoma.

Chevalone C is a meroterpenoid fungal metabolite originally isolated from E. chevalieri. It is active against M. tuberculosis H37Ra (MIC = 6.3 μg/ml) and is cytotoxic to BC1 human breast cancer cells (IC50 = 8.7 μg/ml). Chevalone C inhibits the growth of multidrug-resistant isolates of E. coli, S. aureus, and E. faecium in a disc diffusion assay when used at a concentration of 15 μg/disc. It also induces cell death in HCT116 colorectal carcinoma cells.

BRD4/CK2-IN-1 is a small molecule inhibitor targeting BRD4 and CK2, with an IC50 of 180nM for BRD4 and 230nM for CK2. It inhibits the proliferation of MDA-MB-231 and MDA-MB-468 cells, inducing apoptosis and autophagy-related cell death. It can be used in triple-negative breast cancer research.