2. Metabolic Enzyme/Protease Apoptosis Epigenetics Cell Cycle/DNA Damage
  3. Aminoacyl-tRNA Synthetase Apoptosis Caspase PARP c-Myc
  4. NCP26

NCP26 is an ATP-competitive ProRS inhibitor (with a KD of 271 nM in the absence of proline, and a KD of 0.35 nM in the presence of 100 μM proline). NCP26 activates AAR, induces G0/G1 phase arrest, Apoptosis, Caspase cleavage, and PARP cleavage. NCP26 downregulates MYC, TCF3, and CCND1. NCP26 inhibits the growth of multiple myeloma cells. NCP26 can be used for the research of multiple myeloma.

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

NCP26

NCP26 Chemical Structure

CAS No. : 2396683-89-7

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NCP26 Related Antibodies

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PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

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Description

NCP26 is an ATP-competitive ProRS inhibitor (with a KD of 271 nM in the absence of proline, and a KD of 0.35 nM in the presence of 100 μM proline). NCP26 activates AAR, induces G0/G1 phase arrest, Apoptosis, Caspase cleavage, and PARP cleavage. NCP26 downregulates MYC, TCF3, and CCND1. NCP26 inhibits the growth of multiple myeloma cells. NCP26 can be used for the research of multiple myeloma[1][2].

IC50 & Target[1]

Caspase 8

 

Caspase 9

 

Caspase 3

 

In Vitro

NCP26 is an ATP-competitive inhibitor of recombinant ProRS. Its binding affinity increases by more than 750-fold in the presence of 100 μM proline, with a KD of 0.35 nM[1].
NCP26 (0.5 μM; 48 h) maintains antiproliferative activity against AMO1 and RPMI 8226 multiple myeloma (MM) cells over a proline concentration range of 0 to 20 mM, with no reduction in its potency at high proline levels[1].
NCP26 (0.01-10 μM; 96 h) is 10-fold more potent against AMO1 multiple myeloma (MM) cells than against peripheral blood mononuclear cells (PBMCs) from healthy donors, with an EC50 of 0.1 μM for the former and approximately 1 μM for the latter after 96 h of treatment[1].
NCP26 potently inhibits the growth of most multiple myeloma (MM) cell lines, with EC50 values ranging from 135 nM to 1.1 μM[1].
NCP26 (0.5 μM; 6-48 h) induces G0/G1 cell cycle arrest and caspase-dependent apoptosis in AMO1 and RPMI 8226 multiple myeloma (MM) cells[1].

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

NCP26 Related Antibodies

Cell Cycle Analysis[1]

Cell Line: AMO1, RPMI 8226 MM cell lines
Concentration: 0.5 μM
Incubation Time: 6 h, 24 h, 48 h
Result: Induced G0/G1 cell cycle arrest in both cell lines at 6 h, with enhanced arrest observed at 24 h.
Induced apoptotic cell death, evidenced by increased Annexin-V+ cells, sub-G1 populations, and mitochondrial damage.
Induced time- and dose-dependent cleavage of caspases-3, -8, -9, and PARP.

Western Blot Analysis[1]

Cell Line: AMO1, RPMI 8226 MM cell lines
Concentration: 0-1 μM
Incubation Time: 6 h
Result: Dose-dependently reduced protein levels of MYC, PIM2, CCND1, and TCF3 in both cell lines.
Mirrored the effects of EPRS shRNA knockdown on MYC, PIM2, CCND1, and TCF3 protein levels.
In Vivo

NCP26 (2.5-10 mg/kg; i.p.; once daily; 21 days) significantly inhibits multiple myeloma tumour growth (P = 0.01 and P < 0.001, respectively) and prolongs overall survival (P = 0.01 and P < 0.001, respectively) in CB17 SCID mice bearing AMO1 xenografts, without causing significant body weight loss[1].
NCP26 (10 mg/kg; q.d. [daily]) significantly inhibits multiple myeloma tumor growth (P = 0.005) and prolongs host survival (P < 0.001) in an AMO1 xenograft mouse model without inducing weight loss[2].

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

Animal Model: CB17 SCID (5-week-old female, subcutaneously inoculated with AMO1 cells)[1]
Dosage: 2.5 mg/kg; 10 mg/kg
Administration: i.p.; once daily; 21 days
Result: Significantly inhibited AMO1 tumour growth compared to vehicle control (control vs.
2.5 mg/kg, P = 0.01; control vs.
10 mg/kg, P < 0.001).
Resulted in greater tumour growth inhibition at 10 mg/kg dose than 2.5 mg/kg dose.
Caused no significant body weight loss in either treatment cohort.
Significantly prolonged overall survival compared to vehicle control (control vs.
2.5 mg/kg, P = 0.01; control vs.
10 mg/kg, P < 0.001).
Downregulated MYC, CCND1, and TCF3, and induced p-GCN2 and DDIT3 in treated tumours.
Molecular Weight

365.44

Formula

C20H23N5O2
CAS No.
SMILES

O=C(NC1CC=2C=CC=CC2C1)C3=NC=CN=C3NC(=O)N4CCCCC4
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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NCP26 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    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:

NCP262396683-89-7NCP 26NCP-26Aminoacyl-tRNA SynthetaseApoptosisCaspasePARPc-MyctRNA Synthetase, aaRSpoly ADP ribose polymerase MycISRAMO1ProRSATF4GCN2EPRSeIF2αDDIT3AARmultiple myelomaInhibitorinhibitorinhibit

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