2. JAK/STAT Signaling Stem Cell/Wnt Apoptosis
  3. STAT Apoptosis
  4. Danvatirsen sodium

Danvatirsen sodium  (Synonyms: AZD9150 sodium)

Cat. No.: HY-145729A Purity: 99.46%
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Danvatirsen sodium (AZD9150 sodium) is an antisense oligonucleotide targeting STAT3. Danvatirsen sodium reduces the viability and promotes apoptosis of leukemia cell lines. Danvatirsen sodium inhibits the expression of endogenous STAT3 and its downstream target genes, and reduces the proliferation and tumorigenicity of neuroblastoma and lymphoma cells. Danvatirsen sodium inhibited tumor growth in mouse models of neuroblastoma, lymphoma, and non-small cell lung cancer. Danvatirsen sodium achieves STAT3 mRNA and protein depletion in a mouse model of epidermoid carcinoma. Danvatirsen sodium can be used in research related to lymphoma, myelodysplastic syndrome, acute myeloid leukemia, neuroblastoma and non-small cell lung cancer.

For research use only. We do not sell to patients.

DNA, d(P-thio)([(5′ξ)-2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-lyxo-hexofurano]m5C-(3′→4′)-[(5′ξ)-2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-lyxo-hexofurano]m5U-(3′→4′)-[(5′ξ)-2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-lyxo-hexofurano]A-T-T-T-G-G-A-T-G-T-m5C-(3′→4′)-[(5′ξ)-2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-lyxo-hexofurano]A-(3′→4′)-[(5′ξ)-2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-lyxo-hexofurano]G-(3′→4′)-[(5′ξ)-2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-lyxo-hexofurano]m5C), sodium salt

Danvatirsen sodium Chemical Structure

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Description

Danvatirsen sodium (AZD9150 sodium) is an antisense oligonucleotide targeting STAT3. Danvatirsen sodium reduces the viability and promotes apoptosis of leukemia cell lines. Danvatirsen sodium inhibits the expression of endogenous STAT3 and its downstream target genes, and reduces the proliferation and tumorigenicity of neuroblastoma and lymphoma cells. Danvatirsen sodium inhibited tumor growth in mouse models of neuroblastoma, lymphoma, and non-small cell lung cancer. Danvatirsen sodium achieves STAT3 mRNA and protein depletion in a mouse model of epidermoid carcinoma. Danvatirsen sodium can be used in research related to lymphoma, myelodysplastic syndrome, acute myeloid leukemia, neuroblastoma and non-small cell lung cancer[1][2][3][4].

In Vitro

Danvatirsen (2.5-10 μM) sodium significantly reduces STAT3 mRNA levels in KG1a, CMK, MOLM13 and KT1 leukemia cell lines[2].
Danvatirsen (1-10 μM; 24-72 h) sodium significantly reduces the viability of leukemia/myelodysplastic syndrome (MDS) cell lines including NB4, MOLM14, MDS-L, MV411, KG1a, MOLM13, KT1 and CMK[2].
Danvatirsen (5 μM for CMK, 10 μM for KT1 and U937; 48 h) sodium significantly increases the apoptosis levels of CMK, KT1 and U937 leukemia cell lines[2].
Danvatirsen (2.5-10 μM; 24 h) sodium significantly reduces STAT3 mRNA levels in primary MDS/AML stem cells[2].
Danvatirsen (10 μM; 14 days) sodium enhances erythroid and myeloid differentiation of primary myelodysplastic syndrome (MDS) stem/progenitor cells[2].
Danvatirsen (10 μM; 24 h) sodium downregulates STAT3 and its downstream oncogenic target genes (IL1RAP, MSI2, MCL1, IL8, CXCR2) at the mRNA level, and reduces the protein levels of STAT3, phosphorylated STAT3 and MCL1 in CMK leukemia cells[2].
Danvatirsen sodium induces dose-dependent apoptosis in primary TP53-mutant MDS/AML stem/progenitor cells and reduces the replating efficiency of primary AML stem and progenitor cells in colony-forming assays[2].
Danvatirsen (0.25-10 μM; 6 days) sodium dose-dependently inhibits STAT3 mRNA expression in SK-N-AS, NGP and IMR32 neuroblastoma cells, with IC50 values of 0.69, 0.64 and 0.76 μM, respectively[3].
Danvatirsen (0.25-10 μM; 6 days) sodium dose-dependently inhibits the expression of total STAT3 protein and phosphorylated STAT3 protein in SK-N-AS, NGP and IMR32 neuroblastoma cells, with IC50 values of 0.99 μM, 0.97 μM and 0.98 μM, respectively[3].
Danvatirsen (1 μM; 6 days) sodium significantly reduces the mRNA and protein expression levels of multiple STAT3 target genes in SK-N-AS, NGP and IMR32 neuroblastoma cells[3].
Danvatirsen (1 μM; 4 weeks) sodium significantly inhibits the proliferation of SK-N-AS, NGP and IMR32 neuroblastoma cells, reducing the maximum cell confluence by up to 38%, 37% and 34% respectively during continuous incubation. It also suppresses the anchorage-independent colony formation of the cells, decreasing the number of colonies by 20%, 43% and 67% respectively[3].
Danvatirsen (1 μM; 6 days) sodium significantly enhances the sensitivity of SK-N-AS, NGP and IMR32 neuroblastoma cells to Cisplatin (HY-17394), reduces the IC50 value of Cisplatin by up to 2-fold, and attenuates the activation of Cisplatin-induced DNA damage response pathways[3].
Danvatirsen (0.005-5 μM; 5 days) sodium dose-dependently inhibits the proliferation of STAT3-dependent human lymphoma cell lines KARPAS299 and SUP-M2 via free uptake[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Danvatirsen sodium Related Antibodies

Cell Viability Assay[2]

Cell Line: NB4, MOLM14, MDS-L, MV411, KG1a, MOLM13, KT1, CMK leukemic/MDS cell lines
Concentration: 10 μM
Incubation Time: 24 h, 48 h, 72 h
Result: Induced a significant, dose-dependent decrease in cell viability across all tested cell lines.
Showed greater inhibition at higher concentrations.

Apoptosis Analysis[2]

Cell Line: CMK, KT1, U937 leukemic cell lines
Concentration: 5 μM (CMK cells); 10 μM (KT1 and U937 cells)
Incubation Time: 48 h
Result: Induced a significant increase in early apoptotic, late apoptotic, and necrotic cell populations compared with controls.
Showed a dose-dependent effect observed across tested concentrations.

Real Time qPCR[2]

Cell Line: CMK leukemic cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Downregulated expression of STAT3 and oncogenic/stem cell-associated genes including IL1RAP, MSI2, MCL1, IL8, and CXCR2 at the mRNA level.

Western Blot Analysis[2]

Cell Line: CMK leukemic cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Reduced STAT3 protein, phospho-STAT3, and MCL1 protein levels.
In Vivo

Danvatirsen (50 mg/kg, s.c., 5 days per week for 4 consecutive weeks) sodium significantly reduces the engraftment rate of human MDS/AML cells in NSG mice[2].
Combination of Danvatirsen (100 mg/kg; s.c.; 5 times per week for 3 consecutive weeks) sodium with Cisplatin results in a maximum growth inhibition rate of 38% in neuroblastoma xenografts and significantly prolongs the survival of tumor-bearing mice[3].
Danvatirsen (25-50 mg/kg; s.c.; 5 times per week; for 3 consecutive weeks) sodium induces potent, dose-dependent depletion of STAT3 mRNA and protein in human epidermoid carcinoma A431 xenografts, with the 25 mg/kg dose reducing tumor STAT3 mRNA levels by 90%[4].
Danvatirsen (50 mg/kg, s.c., 5 times per week for 5 weeks) sodium inhibits the growth of human lymphoma SUP-M2 xenografts with an inhibition rate of 62%, and reduces tumor STAT3 mRNA levels by approximately 40%. It exhibits systemic anti-lymphoma activity in the disseminated SUP-M2 model, reducing tumor STAT3 mRNA by approximately 50% and decreasing plasma concentrations of sIL-2Rα and sCD30[4].
Danvatirsen (25 mg/kg; s.c.; 5 times per week; for approximately 5 weeks) sodium inhibits the growth of PC-9 human non-small cell lung cancer xenografts by 90%, and reduces STAT3 activity and the expression of its downstream target genes[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Nonobese Diabetic Scid Gamma (NSG) (irradiated, engrafted with primary human MDS/AML peripheral blood mononuclear cells)[2]
Dosage: 50 mg/kg
Administration: s.c.; 5 days per week; 4 weeks
Result: Reduced MDS/AML burden, with greatly decreased fold change of human CD45+ cells in bone marrow compared with controls.
Achieved complete loss of detectable human CD45+ cells in some treated mice.
Exerted effects in both low-risk and high-risk MDS patient-derived xenografts.
Animal Model: athymic nude mice (5-6 week-old female)[3]
Dosage: 100 mg/kg (target reagent); 2 mg/kg (Cisplatin)
Administration: subcutaneous (target reagent; 5 times per week; 3 weeks); intraperitoneal (cisplatin; 2 times per week; 3 weeks; co-administered starting on day 11 of target reagent treatment)
Result: Reduced neuroblastoma xenograft growth by up to 38% compared to control-treated mice.
Prolonged survival significantly compared to control-treated mice.
Animal Model: Immunocompromised mice; NSG mice (disseminated lymphoma model)[4]
Dosage: 25 mg/kg; 37.5 mg/kg; 50 mg/kg
Administration: 5 times per week; 3 weeks (25 mg/kg, 50 mg/kg)
Result: Reduced tumor STAT3 mRNA by approximately 90% (P=0.0001) and STAT3 protein by 93% (25 mg/kg).
Produced near-complete depletion of STAT3 protein throughout the tumor as measured by immunohistochemistry (50 mg/kg).
Animal Model: NSG mice, Immunocompromised mice[4]
Dosage: 50 mg/kg
Administration: 5 times per week; 2, 5 weeks
Result: Reduced STAT3 mRNA by ~50% in tumors isolated from axillary lymph nodes and peritoneal cavity vs control groups.
Reduced plasma sIL-2Rα and sCD30 concentrations.
Reduced tumor burden (and ascites formation.
Achieved 67% tumor growth inhibition (TGI).
Confirmed inhibition of human STAT3 in tumor cells and murine STAT3 in tumor-associated stromal cells via species-specific PCR.
Confirmed reduced phospho-STAT3 protein in both human tumor and mouse stromal cells via immunohistochemistry.
No associated change in body weight was observed.
Animal Model: Immunocompromised mice[4]
Dosage: 25 mg/kg
Administration: 5 times per week; ~5 weeks
Result: Achieved 90% tumor growth inhibition (TGI) vs control .
Reduced tumor STAT3 and phospho-STAT3 protein, and reduced expression of STAT3 target genes c-MYC, MCL-1, and VEGF.
Molecular Weight

5422 (free acid)

Appearance

Solid

Color

White to light yellow

SMILES

[Danvatirsen (sodium)]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Purity & Documentation

Purity: 99.46%

SDS (251 KB)

COA (246 KB) LCMS (316 KB)

Handling Instructions (2242 KB)
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

DanvatirsenAZD9150AZD 9150AZD-9150STATApoptosisSTAT3 InhibitorMOLM14 cellsMDS-L cellsMV411 cellsKG1a cellsMOLM13 cellsKT1 cellsCMK leukemic/MDS cell linesSK-N-AS cellsNGP cellsIMR32 cellslymphomamyelodysplastic syndromeacute myeloid leukemianeuroblastoma and non-small cell lung cancerInhibitorinhibitorinhibit

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