Apoptosis Compound Library

Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions, which is also called programmed cell death (PCD). Apoptosis plays a crucial role in developing and maintaining the health of the body by eliminating old cells, unhealthy cells and unnecessary cells. Too little or too much apoptosis contribute to many diseases. When apoptosis does not work correctly, cells that should be eliminated may persist and become immortal, for example, in cancer and leukemia. When apoptosis works overly well, it kills too many cells and inflicts grave tissue damage. This is the case in strokes and neurodegenerative disorders such as Alzheimer's, Huntington's, and Parkinson's disease.

MCE designs a unique collection of 3,590 apoptosis-related compounds mainly focusing on the key targets in the apoptosis signaling pathway and can be used in the research of apoptosis signal pathway and related diseases.

Energy metabolism is the most fundamental biochemical process in living organisms, encompassing glycolysis, the TCA cycle, oxidative phosphorylation, the pentose phosphate pathway, and fatty acid oxidation. These core pathways directly regulate cell survival, proliferation, differentiation, and apoptosis. Dysregulation of energy metabolism is closely linked to major diseases including cancer, diabetes, obesity, cardiovascular diseases, neurodegenerative disorders, and ischemia‑reperfusion injury. Targeting these metabolic pathways has become a frontier in drug discovery and mechanistic research.

The MCE Energy Metabolite Compound Library features 70 structurally defined small‑molecule compounds. It covers energy substrates, pathway intermediates, coenzymes and redox carriers, nucleotide derivatives, and microenvironmental modulators. This library is applicable to research areas including tumor metabolism, insulin resistance, mitochondrial dysfunction, oxidative stress, neuroprotection, and cardiometabolic diseases, providing a high‑quality tool for mechanistic studies, biomarker discovery, and high‑throughput drug screening.

Ferroptosis is a novel type of cell death program that is distinct from apoptosis, necroptosis and autophagy. It is dependent on iron and reactive oxygen species (ROS) and is characterized by lipid peroxidation. As a novel type of cell death, ferroptosis has distinct properties and recognizing functions involved in physical conditions or various diseases including cancers, neurodegenerative diseases, acute renal failure, etc.

MCE carefully collected a unique collection of 1,232 ferroptosis signaling pathway related compounds with ferroptosis-inducing or -inhibitory activity. MCE Ferroptosis Compound Library is a useful tool to study ferroptosis mechanism as well as related diseases.

Protein ubiquitination is an enzymatic post-translational modification in which an ubiquitin protein is attached to a substrate protein. Ubiquitination involves three main steps: activation, conjugation, and ligation, performed by ubiquitin-activating enzymes (E1s), ubiquitin-conjugating enzymes (E2s), and ubiquitin ligases (E3s), respectively. Ubiquitination affects cellular processes such as apoptosis, cell cycle, DNA damage repair, and membrane transportation, etc. by regulating the degradation of proteins (via the proteasome and lysosome), altering the cellular localization of proteins, affecting proteins activity, and promoting or preventing protein-protein interactions. Deregulation of ubiquitin pathway leads to many diseases such as neurodegeneration, cancer, infection and immunity, etc.

MCE offers a unique collection of 494 small molecule modulators with biological activity used for ubiquitination research. Compounds in this library target the key enzymes in ubiquitin pathway. MCE Ubiquitination Compound Library is a useful tool for the research of ubiquitination regulation and the corresponding diseases.

Parkinson’s disease (PD), the second most common age-associated neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons and the presence of α-synuclein-containing aggregates in the substantia nigra pars compacta (SNpc). Motor features such as tremor, rigidity, bradykinesia and postural instability are common traits of PD. To date, there is no treatment to stop or at least slow down the progression of the disease. The etiology and pathogenesis of PD is still elusive, however, a large body of evidence suggests a prominent role of oxidative stress, inflammation, apoptosis, mitochondrial dysfunction and proteasome dysfunction in the pathogenesis of PD.

MCE offers a unique collection of 2,158 compounds with anti- Parkinson’s Disease activities or targeting the unique targets of PD. MCE Anti- Parkinson's Disease Compound Library is a useful tool for exploring the mechanism of PD and discovering new drugs for PD.

Mitochondria plays an important role in many vital processes in cells, including energy production, fatty-acid oxidation and the Tricarboxylic Acid (TCA) cycle, calcium signaling, permeability transition, apoptosis and heat production. At present, it is recognized that many diseases are associated with impaired mitochondrial function, such as increased accumulation of ROS and decreased OXPHOS and ATP production. Mitochondria are recognized as one of the most important targets for new drug design in cancer, cardiovascular, and neurological diseases, etc. Some small molecule drugs or biologics can act on mitochondria through various pathways, including ETC inhibition, OXPHOS uncoupling, mitochondrial Ca²⁺ modulation, and control of oxidative stress via decrease or increase of mitochondrial ROS accumulation.

MCE supplies a unique collection of 1,169 mitochondria-targeted compound that mainly targeting Mitochondrial Metabolism, ATP Synthase, Mitophagy, Reactive Oxygen Species, etc. MCE Mitochondria-Targeted Compound Library is a useful tool for mitochondria-targeted drug discovery and related research.

With the progress of modern cancer therapy, the life of cancer patients has been extended. However, after initial treatment and recovery, the development of secondary tumors often leads to cancer recurrence. Cancer stem cells are a small number of cells that tumor growth and reproduction depend on.

Cancer stem cells have strong self-renewal ability, which is the direct cause of tumor occurrence. In addition, cancer stem cells also have the ability to differentiate into different cell types, playing a crucial role in tumor metastasis and development. Chemotherapy and radiotherapy induced DNA damage and apoptosis are common cancer treatments. However, cancer stem cells can effectively protect cancer cells from apoptosis by activating DNA repair ability. Cancer stem cells are regarded as the key "seed" of tumor occurrence, development, metastasis and recurrence. Since its first discovery in leukemia in 1994, cancer stem cells have been considered a promising therapeutic target for cancer treatment.

MCE supplies a unique collection of 3,499 compounds targeting key proteins in cancer stem cells. MCE Cancer Stem Cells Compound Library is a useful tool for cancer stem cells related research and anti-cancer drug development.

The transforming growth factor beta (TGF-β) signaling pathway is involved in many cellular processes in both the adult organism and the developing embryo including cell growth, cell differentiation, apoptosis, cellular homeostasis and other cellular functions. The TGF-β superfamily comprises TGF-βs, bone morphogenetic proteins (BMPs), activins and related proteins. Signaling begins with the binding of a TGF beta superfamily ligand to a TGF beta type II receptor. The type II receptor is a serine/threonine receptor kinase, which catalyzes the phosphorylation of the Type I receptor. The type I receptor then phosphorylates receptor-regulated SMADs (R-SMADs) which can now bind the coSMAD (e.g. SMAD4). R-SMAD/coSMAD complexes accumulate in the nucleus where they act as transcription factors and participate in the regulation of target gene expression. Deregulation of TGF-β signaling contributes to developmental defects and human diseases, including cancers, some bone diseases, chronic kidney disease, etc.

MCE designs a unique collection of 449 TGF-beta/Smad signaling pathway compounds. TGF-beta/Smad Compound Library acts as a useful tool for TGF-beta/Smad-related drug screening and disease research.

The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials.

MCE owns a unique collection of 1,125 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis".

The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis.

Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism.

Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis.

MCE supplies a unique collection of 440 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.