1. Epigenetics
    Stem Cell/Wnt
    JAK/STAT Signaling
    Protein Tyrosine Kinase/RTK
  2. JAK

Cerdulatinib (Synonyms: PRT062070; PRT2070)

Cat. No.: HY-15999 Purity: 97.44%
Data Sheet SDS Handling Instructions

Cerdulatinib is a novel, orally available, ATP-competitive inhibitor that demonstrates selective inhibition of SYK and JAK kinases with IC50 of 32 nM for SYK and 0.5-12 nM for JAKs.

For research use only. We do not sell to patients.
Cerdulatinib Chemical Structure

Cerdulatinib Chemical Structure

CAS No. : 1198300-79-6

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10 mM * 1 mL in DMSO $99 In-stock
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10 mg $120 In-stock
50 mg $400 In-stock
100 mg $620 In-stock
200 mg $920 In-stock
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  • Biological Activity

  • Protocol

  • Technical Information

  • Purity & Documentation

  • References


Cerdulatinib is a novel, orally available, ATP-competitive inhibitor that demonstrates selective inhibition of SYK and JAK kinases with IC50 of 32 nM for SYK and 0.5-12 nM for JAKs.

IC50 & Target

IC50: 32 nM (SYK), 0.5-12 nM (JAKs)[1], 12 nM (JAK1)[3]

In Vitro

Cerdulatinib shows inhibitory effect on 60 CLL with IC50 ranging from 0.37 to 10.02 µM. Cerdulatinib induces apoptosis in CLL in association with MCL-1 down-regulation and PARP cleavage. Cerdulatinib (2μM) is able to overcome the support of the microenvironment and induces CLL cell death. Cerdulatinib (250-500 nM) blocks proliferation of ibrutinib-sensitive and ibrutinib-resistant primary CLL cells. Cerdulatinib also blocks proliferation of both ibrutinib-sensitive and ibrutinib-resistant primary CLL cells as well as BTKC481S-transfected cell lines, and blocks BCR and JAK-STAT signaling pathways. Furthermore, inhibition of SYK and JAK by cerdulatinib translates to downstream inhibition of AKT and ERK. Cerdulatinib inhibits the activity of NF-kB pathway[1]. PRT062070 reduces the ability of stimulated B cells to upregulate cell-surface expression of the early activation marker CD69 (IC50=0.11 µM). PRT062070 exhibits differential potency against cytokine JAK/STAT signaling pathways. PRT062070 (1 or 3 µM) induces apoptosis in BCR-signaling competent NHL cell lines[2]. Cerdulatinib demonstrates inhibitory activity against both ABC and GCB subtypes of DLBCL cells. Cerdulatinib also induces apoptosis in both GCB and ABC subtypes of DLBCL cell lines via caspase 3 and PARP cleavage. And cerdulatinib blocks cell cycle in both ABC and GCB subtypes of DLBCL via inhibition of RB phosphorylation and down-regulation of cyclin E. Cerdulatinib induces cell cycle arrest and apoptosis under the condition of BCR stimulation in all DLBCL cell lines. Besides, cerdulatinib blocks JAK/STAT and BCR signaling in both ABC and GCB DLBCL cell lines. Cerdulatinib induces cell death in primary human DLBCL samples[3]. Cerdulatinib inhibits BCR-induced signals in a dose-dependent manner and most strongly between 0.3 to 1 μM. and particularly in IGHV-unmutated samples with greater BCR signaling capacity and response to IL4, or samples expressing higher levels of sIgM, CD49d+, or ZAP70+. Cerdulatinib overcomes anti-IgM, IL4/CD40L, or NLC-mediated protection by preventing upregulation of MCL-1 and BCL-XL; however, BCL-2 expression is unaffected. Furthermore, in samples treated with IL4/CD40L, cerdulatinib synergizes with venetoclax in vitro to induce greater apoptosis than either drug alone[4].

In Vivo

PRT062070 (0.5 mg/kg) results in a nonstatistically significant trend toward reduced ankle inflammation, whereas significant reductions in inflammation are achieved with the 1.5, 3, and 5 mg/kg doses. PRT062070 also affects anticollagen antibody formation. PRT062070 (15 mg/kg) suppresses upregulation of splenic B-cell surface CD80/86 and CD69, and inhibits BCR signaling and activation in the spleen after oral dosing in mice[2].

Clinical Trial
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Preparing Stock Solutions
Concentration Volume Mass 1 mg 5 mg 10 mg
1 mM 2.2445 mL 11.2223 mL 22.4447 mL
5 mM 0.4489 mL 2.2445 mL 4.4889 mL
10 mM 0.2244 mL 1.1222 mL 2.2445 mL
Please refer to the solubility information to select the appropriate solvent.
Cell Assay

Cerdulatinib is dissolved in DMSO.

TMD8 cells are transfected with constructs of WT BTK or BTKC481S mutants using kit V, Program U-13 on Amaxa Nucleofector. After transfection, the cells are co-cultured with NKTert cells in a 24-well plate for 24 hrs for recovery. Ibrutinib, cerdulatinib and vehicle (DMSO) are then added into the transfected TMD8 cells and cellular viability is determined with MuseTM Count & Viability kit using Muse Cell Analyzer. The cell survival is determined by flow cytometry using the Annexin V/7-AAD Apoptosis Detection Kit I on freshly isolated CLL cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Molecular Weight






Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month

Room temperature in continental US; may vary elsewhere

Solvent & Solubility

DMSO: ≥ 30 mg/mL

* "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

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