IVD Raw Materials
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About Us
Compound Libraries


WBWestern Blotting




FCFlow Cytometry



DBDot Blotting

ChIPChromatin Immunoprecipitation

GICAGold Immunochromatography Assay

NCNegative Control

Species Reactivity




Dm Drosophila melanogaster

C Caenorhabditis elegans



B Bovine 

D Dog



ChHm Chinese Hamster 



Phosphatase inhibitor libraryL9100


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Apoptosis Compound LibraryL9000

Brief: Apoptosisis a form ofprogrammed cell deaththat occurs inmulticellular organisms. In contrast tonecrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis is a highly regulated and controlled process that confers advantages during an organism's lifecycle. Apoptosis leads to characteristic cell changes (morphology): the cell breaks apart into multiple vesicles calledapoptotic bodies, which undergo phagocytosis. Apoptosis is regulated by both pro-apoptotic (such as Fas receptor and caspases) and anti-apoptotic (such as Bcl-2 and IAP) factors. Disordered apoptosis is implicated in a variety of human diseases. Inhibition ofapoptosiscan result in a number of cancers, autoimmunediseases, inflammatory diseases, and viral infections.Excessive apoptosis may also be a feature of some conditions such as autoimmune diseases, neurodegenerative diseases, and ischemia-associated injury.Consequently, considerable interest has arisen in therapeutic strategies for cancer, autoimmune diseases, and neurodegenerative diseases by modulating apoptosis pharmacologically. SABs collection of 191 apoptosis-related compounds, Apoptosis Compound Library, is divided accordingly with compounds designed for either pro- or anti-apoptosis purposes and can be used for research in cancer and neurodegenerative diseases.

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hematonosis compound libraryL8400

Brief: Hematologic diseases (hematonosis), disorders of the blood and blood-forming organs, afflict millions of Americans. In addition to hematological malignancies, such as leukemia and lymphomas, children and adolescents can suffer blood disorder, that are not classified as cancer, but may lead to severe diseases and therefore require treatment. These blood disorders include severe aplastic anemia (SAA), thalassemia, immune (idiopathic) thrombocytopenic purpura, congenital neutropenia, hemophilia, sickle-cell disease, iron deficiency anemia and various other diseases. In the past, due to the lack of effective treatments, many diseases have been called "incurable diseases". In recent years, with in-depth development of medical research, the treatment of blood diseases has been significantly improved. Modern medicine uses hormones, chemotherapy and other methods for the treatment of blood diseases, but the side effects are large, and the patient has a low cure rate and is prone to recurrence. Bone marrow transplantation for the treatment of leukemia was introduced then the cure rate of leukemia was improved. However, the bone marrow resources were very scarce, and a large part of the donated bone marrow was inconsistent with the patient's HLA, even if the transplant was successful, and the recurrence rate was as high as 70% within 5 years. Therefore, it is necessary to develop new therapies and drugs for the treatment of hematologic diseases. Hematonosis Compound Library from SAB provides you with compounds related to hematologic diseases that can be used for high throughput and high content screening.

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Chromatin modification compound libraryL8300

Brief: Chromatin modification, also called Chromatin remodeling, is the rearrangement of chromatin from a condensed state to a transcriptionally accessible state, allowing transcription factors or other DNA binding proteins to access DNA and control gene expression. Such remodeling is principally carried out by 1) covalent histone modifications by specific enzymes, e.g., histone acetyltransferases (HATs), deacetylases, methyltransferases, and kinases, and 2) ATP-dependent chromatin remodeling complexes which either move, eject or restructure nucleosomes. Chromatin remodeling is highly implicated in epigenetics.Epigenetic modifications to histone proteins such as methylation/demethylation and acetylation/deacetylation can alter the structure of chromatin resulting in transcriptional activation or repression. Aberrations in chromatin remodeling proteins are found to be associated with human diseases, including cancer. Targeting chromatin remodeling pathways is currently evolving as a major therapeutic strategy in the treatment of several cancers. Chromatin Modification Compound Library from SAB is a unique collection of 192 compounds targeting chromatin remodeling pathways that can be used for high throughput and high content screening

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Anti-aging Compound LibraryL8200

Brief: Aging is a natural process of becoming older. The causes of aging are assigned to programmed and damage or error theories. The programmed theories imply that aging relies on specific gene regulation, and the damage or error theories emphasize the internal and environmental damages accumulated to living organisms. The damage theories proposed the nine hallmarks that were generally considered to contribute to the aging process: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. There is great interest in finding drugs capable of extending human lifespan and healthspan.Compounds are sought that are capable of modulating multiple aging pathways, thereby preventing a broad-spectrum of age-related diseases. The SABsAnti-Aging Compound Library, a unique collection of 833 anti-aging compounds, is an effective tool for anti-aging research, and anti-aging drug screening

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Cell cycle compound LibraryL8100

Brief: Cell cycle, the ordered sequence of events that occur in acellin preparation forcell division, is also divided into two periods:interphase and themitotic(M) phase. Interphase itself is split into different phases: G1 phase, S phase and G2 phase. Cell Cycle related compounds rely on differing mechanisms of action to regulate the normal progression of the cell cycle. Some of these compounds interfere with CDK/cyclin complexes leaving cells stuck at the G2/M phase border, while others affect CaMKII phosphorylation, inducing arrest at the G1phase. Other mechanisms of action include interference with RNA function and inhibition of protein synthesis. Many of these compounds ultimately induce apoptosis as a result of their interruption of the cell cycle.This library can be used for anti-cancer drug screening.

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Stem cell Differentiation Compound LibraryL8000

Brief: Stem cellscandifferentiateinto other types of cells and candivideto produce more of the same type of stem cells. For example, embryonic stem cells can differentiate into all the specialized cells��ectoderm, endoderm and mesoderm. Somatic stem cells are thought to be limited to differentiating into different celltypes of their tissue of origin. To generate enough specialized cells or tissues that can be used for specific purposes such astissue regeneration, cell-based therapies, drug screening, or disease models, scientists (must control the cell fate of pluripotent stem cells) are currently working on methods to effectivelydifferentiate stem cellsinto functional specializedcells. Natural and synthetic small molecules have been shown to be useful chemical tools for controlling and manipulating the fates of cells. For example, Glycogen synthase kinase 3�� (GSK-3��) inhibitor could induce differentiation of neural progenitor cells (NPCs). Bone marrow stromal stem cells (BMSSCs) may have potential to differentiate in vitro and in vivo into hepatocytes following the treatment of inhibitor of histone deacetylase and some well-defined cytokines. Stem Cell Differential Compound Library from SAB, a unique collection of 340 stem cell differentiation signaling targeted compounds, can be used for stem cell research and related drug screening (high throughput and high content screening).

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Osteogenesis-related compound libraryL7900

Brief: Bone tissue is continuously remodeled through the concerted actions of bone cells, which include bone resorption by osteoclasts and bone formation by osteoblasts. The equilibrium between bone formation and resorption is necessary and depends on the action of several local and systemic factors including hormones, cytokines, chemokines, and biomechanical stimulation.An imbalance between bone resorption and formation can result in bone diseases including osteoporosis.Osteoblasts are the main functional cells of bone formation and are responsible for the synthesis, secretion and mineralization of bone matrix. Osteoblasts undergo four stages of osteoblast proliferation, extracellular matrix maturation, extracellular matrix mineralization, and osteoblast apoptosis during bone formation. Many factors are involved in these stages to ultimately regulate bone formation. Multiple signaling pathways were found to be involved in osteogenic proliferation and differentiation. Among them, BMP-SMAD, Wnt/��-Catenin, Notch, Hedgehog, MAPK, and FGF signaling pathways play the most critical roles in regulating osteogenic differentiation. Osteogenesis Compound Library from SAB collects 80 reported osteogenesis related bioactive compounds that can be used for research in bone formation and drug screening.

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Fragment Compound Library plusL7800


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Neural regeneration compound libraryL7700

Brief: It is well known that neurological diseases that affect the brain or other components of the central nervous system are among the most devastating and complex conditions plaguing mankind today. For thousands of years, damage to the adult central nervous system (CNS) in humans has been regarded as an ��ailment which cannot be treated��. In the adult mammalian CNS, most injured axons do not regenerate, reflecting a major hurdle for functional recovery after trauma. Numerous efforts over more than a century have been devoted to uncover the underlying mechanisms of regeneration failure. The discovery of neural and glial precursor cells in the adult brain and their ability to grow after injury trumped this assumption. However, in most cases, only small numbers of injured CNS axons can regenerate, consistent with the idea that lack of regeneration in the adult CNS is an intrinsic property of the injured neurons. Therefore, a major challenge has been to define the underlying cellular and molecular mechanisms that determine neuronal intrinsic regenerative ability, with the goal to construct a foundation for designing therapeutic neural repair strategies. Many signaling pathways (including Ras homolog gene/Rho-associated coiled coil-forming protein kinase (Rho-ROCK), Notch, MAPK, Wnt/��-catenin, mTOR, and ephephrin) participate in and affect repair or regeneration of neurons and axons in the central nervous system. The cyclic adenosine monophosphate-protein kinase A (cAMP-PKA) and Rho-ROCK signaling pathways are key signal transduction pathways for regulating neural and axonal regeneration. SAB collects 149 compounds related to neuroregeneration as Neuroregeneration Compound Library, which can be used for screening of drugs that promote axonal growth and regeneration

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