EasySep™ Human CD138 Positive Selection Kit II

Immunomagnetic positive selection cell isolation kit

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From: 690 USD


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Immunomagnetic positive selection cell isolation kit
From: 690 USD

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The EasySep™ Human CD138 Positive Selection Kit II is designed to isolate CD138+ (syndecan-1) cells from fresh or previously frozen bone marrow or peripheral blood mononuclear cells by positive selection. Desired cells are targeted with Tetrameric Antibody Complexes recognizing CD138 and dextran-coated magnetic particles. This cocktail also contains an antibody to human Fc receptor to minimize nonspecific binding. Labeled cells are separated using an EasySep™ magnet without the use of columns. Cells of interest remain in the tube while unwanted cells are poured off. The CD138 antigen is expressed on normal and malignant plasma cells (but not mature B cells).

This product is an improved version of the EasySep™ Human CD138 Positive Selection Kit (Catalog #18357) that provides highly purified cells using a shorter protocol.
• Fast and easy-to-use
• No columns required
  • EasySep™ Human CD138 Positive Selection Kit II (Catalog #17877)
    • EasySep™ Human CD138 Positive Selection Kit II Cocktail, 1 mL
    • EasySep™ Dextran RapidSpheres™ 50100, 1 mL
  • RoboSep™ Human CD138 Positive Selection Kit II with Filter Tips (Catalog #17877RF)
    • EasySep™ Human CD138 Positive Selection Kit II Cocktail, 1 mL
    • EasySep™ Dextran RapidSpheres™ 50100, 1 mL
    • RoboSep™ Buffer (Catalog #20104)
    • RoboSep™ Filter Tips (Catalog #20125)
Magnet Compatibility:
• EasySep™ Magnet (Catalog #18000)
• “The Big Easy” EasySep™ Magnet (Catalog #18001)
• EasyEights™ EasySep™ Magnet (Catalog #18103)
• RoboSep™-S (Catalog #21000)
Cell Isolation Kits
Cell Type:
B Cells; Plasma Cells
Sample Source:
Bone Marrow; PBMC
Selection Method:
Cell Isolation
EasySep; RoboSep
Area of Interest:
Cancer Research; Immunology

Scientific Resources

Educational Materials


Product Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Research Area Workflow Stages for
Workflow Stages

Data and Publications


Starting with thawed PBMCs spiked with a multiple myeloma cell line, U266, the CD138+ cell content of the isolated fraction typically ranges from 93.0 - 98.2%. In the above example, the purities of the start and final isolated fractions are 9.16% and 94.34%, respectively.


Cell death discovery 2019

Prosurvival autophagy is regulated by protein kinase CK1 alpha in multiple myeloma.

M. Carrino et al.


Multiple myeloma (MM) is a tumor of plasma cells (PCs). Due to the intense immunoglobulin secretion, PCs are prone to endoplasmic reticulum stress and activate several stress-managing pathways, including autophagy. Indeed, autophagy deregulation is maladaptive for MM cells, resulting in cell death. CK1alpha, a pro-survival kinase in MM, has recently been involved as a regulator of the autophagic flux and of the transcriptional competence of the autophagy-related transcription factor FOXO3a in several cancers. In this study, we investigated the role of CK1alpha in autophagy in MM. To study the autophagic flux we generated clones of MM cell lines expressing the mCherry-eGFP-LC3B fusion protein. We observed that CK1 inhibition with the chemical ATP-competitive CK1 alpha/delta inhibitor D4476 resulted in an impaired autophagic flux, likely due to an alteration of lysosomes acidification. However, D4476 caused the accumulation of the transcription factor FOXO3a in the nucleus, and this was paralleled by the upregulation of mRNA coding for autophagic genes. Surprisingly, silencing of CK1alpha by RNA interference triggered the autophagic flux. However, FOXO3a did not shuttle into the nucleus and the transcription of autophagy-related FOXO3a-dependent genes was not observed. Thus, while the chemical inhibition with the dual CK1alpha/delta inhibitor D4476 induced cell death as a consequence of an accumulation of ineffective autophagic vesicles, on the opposite, CK1alpha silencing, although it also determined apoptosis, triggered a full activation of the early autophagic flux, which was then not supported by the upregulation of autophagic genes. Taken together, our results indicate that the family of CK1 kinases may profoundly influence MM cells survival also through the modulation of the autophagic pathway.
Blood advances 2018 OCT

An inhibitor of proteasome $\beta$2 sites sensitizes myeloma cells to immunoproteasome inhibitors.

S. Downey-Kopyscinski et al.


Proteasome inhibitors bortezomib, carfilzomib and ixazomib (approved by the US Food and Drug Administration [FDA]) induce remissions in patients with multiple myeloma (MM), but most patients eventually become resistant. MM and other hematologic malignancies express ubiquitous constitutive proteasomes and lymphoid tissue-specific immunoproteasomes; immunoproteasome expression is increased in resistant patients. Immunoproteasomes contain 3 distinct pairs of active sites, $\beta$5i, $\beta$1i, and $\beta$2i, which are different from their constitutive $\beta$5c, $\beta$1c, and $\beta$2c counterparts. Bortezomib and carfilzomib block $\beta$5c and $\beta$5i sites. We report here that pharmacologically relevant concentrations of $\beta$5i-specific inhibitor ONX-0914 show cytotoxicity in MM cell lines similar to that of carfilzomib and bortezomib. In addition, increasing immunoproteasome expression by interferon-$\gamma$ increases sensitivity to ONX-0914 but not to carfilzomib. LU-102, an inhibitor of $\beta$2 sites, dramatically sensitizes MM cell lines and primary cells to ONX-0914. ONX-0914 synergizes with all FDA-approved proteasome inhibitors in MM in vitro and in vivo. Thus, immunoproteasome inhibitors, currently in clinical trials for the treatment of autoimmune diseases, should also be considered for the treatment of MM.
Cancer genetics 2018 DEC

Assessing genome-wide copy number aberrations and copy-neutral loss-of-heterozygosity as best practice: An evidence-based review from the Cancer Genomics Consortium working group for plasma cell disorders.

T. J. Pugh et al.


BACKGROUND Plasma cell neoplasms (PCNs) encompass a spectrum of disorders including monoclonal gammopathy of undetermined significance, smoldering myeloma, plasma cell myeloma, and plasma cell leukemia. Molecular subtypes have been defined by recurrent cytogenetic abnormalities and somatic mutations that are prognostic and predictive. Karyotype and fluorescence in situ hybridization (FISH) have historically been used to guide management; however, new technologies and markers raise the need to reassess current testing algorithms. METHODS We convened a panel of representatives from international clinical laboratories to capture current state-of-the-art testing from published reports and to put forward recommendations for cytogenomic testing of plasma cell neoplasms. We reviewed 65 papers applying FISH, chromosomal microarray (CMA), next-generation sequencing, and gene expression profiling for plasma cell neoplasm diagnosis and prognosis. We also performed a survey of our peers to capture current laboratory practice employed outside our working group. RESULTS Plasma cell enrichment is widely used prior to FISH testing, most commonly by magnetic bead selection. A variety of strategies for direct, short- and long-term cell culture are employed to ensure clonal representation for karyotyping. Testing of clinically-informative 1p/1q, del(13q) and del(17p) are common using karyotype, FISH and, increasingly, CMA testing. FISH for a variety of clinically-informative balanced IGH rearrangements is prevalent. Literature review found that CMA analysis can detect abnormalities in 85-100{\%} of patients with PCNs; more specifically, in 5-53{\%} (median 14{\%}) of cases otherwise normal by FISH and cytogenetics. CMA results in plasma cell neoplasms are usually complex, with alteration counts ranging from 1 to 74 (median 10-20), primarily affecting loci not covered by FISH testing. Emerging biomarkers include structural alterations of MYC as well as somatic mutations of KRAS, NRAS, BRAF, and TP53. Together, these may be measured in a comprehensive manner by a combination of newer technologies including CMA and next-generation sequencing (NGS). Our survey suggests most laboratories have, or are soon to have, clinical CMA platforms, with a desire to move to NGS assays in the future. CONCLUSION We present an overview of current practices in plasma cell neoplasm testing as well as an algorithm for integrated FISH and CMA testing to guide treatment of this disease.
Acta Neuropathologica Communications 2017 dec

CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons

M. Ortiz-Virumbrales et al.


Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval. We present an optimized in vitro protocol to generate human BFCNs from iPSCs, using cell lines from presenilin 2 (PSEN2) mutation carriers and controls. As expected, cell lines harboring the PSEN2 N141I mutation displayed an increase in the A?42/40 in iPSC-derived BFCNs. Neurons derived from PSEN2 N141I lines generated fewer maximum number of spikes in response to a square depolarizing current injection. The height of the first action potential at rheobase current injection was also significantly decreased in PSEN2 N141I BFCNs. CRISPR/Cas9 correction of the PSEN2 point mutation abolished the electrophysiological deficit, restoring both the maximal number of spikes and spike height to the levels recorded in controls. Increased A?42/40 was also normalized following CRISPR/Cas-mediated correction of the PSEN2 N141I mutation. The genome editing data confirms the robust consistency of mutation-related changes in A?42/40 ratio while also showing a PSEN2-mutation-related alteration in electrophysiology.