2. Metabolic Enzyme/Protease Apoptosis
  3. NAMPT Apoptosis
  4. Nampt-IN-17

Nampt-IN-17 is an selective orally active NAMPT inhibitor with a human NAMPT IC50 of 17 nM and Ki of 25.9 nM. Nampt-IN-17 depletes intracellular NAD+ and ATP, disrupts mitochondrial membrane potential, suppresses cell proliferation, self-renewal, invasion, and migration, induces cell-cycle arrest and apoptosis. Nampt-IN-17 exhibits selective activity against NAPRT-deficient gastric cancer cells. Nampt-IN-17 can be used for the research of NAPRT-deficient gastric cancer.

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Nampt-IN-17

Nampt-IN-17 Chemical Structure

CAS No. : 3077970-78-3

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Nampt-IN-17 Related Antibodies

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Description

Nampt-IN-17 is an selective orally active NAMPT inhibitor with a human NAMPT IC50 of 17 nM and Ki of 25.9 nM. Nampt-IN-17 depletes intracellular NAD+ and ATP, disrupts mitochondrial membrane potential, suppresses cell proliferation, self-renewal, invasion, and migration, induces cell-cycle arrest and apoptosis. Nampt-IN-17 exhibits selective activity against NAPRT-deficient gastric cancer cells. Nampt-IN-17 can be used for the research of NAPRT-deficient gastric cancer[1].

In Vitro

Nampt-IN-17 (N16) (varying concentrations; 30 min) potently inhibits recombinant human NAMPT enzyme with an IC50 of 17 nM via a noncompetitive mechanism and exhibits high selectivity for NAMPT over HDACs and most kinases, with moderate inhibition of some CYP450 isoforms, particularly CYP3A4/5[1].
Nampt-IN-17 (3.1-100 μM) directly binds to recombinant human NAMPT with a Kd of 9.17 μM[1].
Nampt-IN-17 (72 h) selectively potently inhibits the viability of NAPRT-deficient gastric cancer cells (HGC-27, MKN-74, MKN-45) with IC50 values ranging from 0.0013 to 0.017 μM, while sparing NAPRT-expressing normal and cancer cells[1].
Nampt-IN-17 (0.1-60 nM; 24-48 h) potently and dose-dependently inhibits proliferation and clonogenicity of NAPRT-deficient HGC-27 and MKN-74 gastric cancer cells[1].
Nampt-IN-17 (0.1-1.6 nM; 24 h) dose-dependently suppresses migration and invasion of NAPRT-deficient HGC-27 gastric cancer cells[1].
Nampt-IN-17 (1.6-6.4 nM; 48 h) induces dose-dependent S-phase and G2/M-phase cell-cycle arrest and apoptosis in NAPRT-deficient HGC-27 gastric cancer cells[1].
Nampt-IN-17 (1.6-6.4 nM; 24-48 h) dose-dependently depletes intracellular NAD+ and ATP levels, and disrupts mitochondrial membrane potential in NAPRT-deficient HGC-27 gastric cancer cells, with effects reversible by NMN but not nicotinic acid[1].

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

Nampt-IN-17 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: NAPRT-deficient gastric cancer cell lines (HGC-27, MKN-74)
Concentration: 0.1, 0.4, 1.6 nM
Incubation Time: 24-48 h (EdU assay)
Result: Dose-dependently suppressed EdU-positive proliferating cells in HGC-27 and MKN-74 cells.
Reduced colony formation in both cell lines.

Cell Migration Assay[1]

Cell Line: NAPRT-deficient gastric cancer cell line (HGC-27)
Concentration: 0.03 nM, 0.1 nM, 0.32 nM, 1 nM, 3.2 nM, 10 nM, 32 nM
Incubation Time: 24, 48, 72 h
Result: Dose-dependently inhibited migration and invasion of HGC-27 cells, with greater activity than lead compound 1 and apatinib at equivalent concentrations.

Cell Cycle Analysis[1]

Cell Line: NAPRT-deficient gastric cancer cell line (HGC-27)
Concentration: 1.6, 3.2, 6.4 nM
Incubation Time: 48 h
Result: Induced concentration-dependent S-phase and G2/M-phase arrest in HGC-27 cells, with 6.4 nM N16 causing 44.3% S-phase and 35.8% G2/M-phase arrest.
Dose-dependently induced apoptosis, with 6.4 nM N16 resulting in 54.6% apoptotic cells, predominantly late apoptosis.

Cell Migration Assay [1]

Cell Line: HGC-27 cells
Concentration: 0.1, 0.4, 1.6 nM
Incubation Time: 24 h
Result: Suppressed the clonogenic potential of gastric cancer cells, reflecting its ability to inhibit long-term cell growth and tumorigenicity.
Parmacokinetics
Species Dose Route T1/2 Tmax Cmax AUC0-∞ MRT0-∞ CL
Rat[1] 2 mg/kg i.v. 0.91 h 0.03 h 14400 μg/L 4155.7 0.33 h 0.48 L/h/kg
Rat[1] 10 mg/kg i.g. 6.32 h 0.67 h 84.07 μg/L 282.9 6.42 h 39.0 L/h/kg
In Vivo

N16 (7.5-15 mg/kg; i.g.; twice daily; 12 days) exhibits dose-dependent in vivo antitumor efficacy against NAPRT-deficient HGC-27 gastric cancer xenografts, with a maximum TGI of 78.9% at 15 mg/kg twice daily[1].

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

Animal Model: BALB/c nude (male; 4-5 weeks old for efficacy study; 6 weeks old for short-term toxicity study; subcutaneous xenograft of NAPRT-deficient HGC-27 cells)[1]
Dosage: 7.5 mg/kg
Administration: i.g.; twice daily; 12 days
Result: Achieved a tumor growth inhibition (TGI) rate of 65.3%, reduced final tumor weight compared to vehicle, and caused no significant body weight loss or organ toxicity (no histological abnormalities in heart, liver, lung, spleen, or kidney).
Animal Model: BALB/c nude (male; 4-5 weeks old for efficacy study; 6 weeks old for short-term toxicity study; subcutaneous xenograft of NAPRT-deficient HGC-27 cells)[1]
Dosage: 15 mg/kg
Administration: i.g.; twice daily; 12 days
Result: Achieved a TGI rate of 78.9%, reduced final tumor weight compared to vehicle, but caused gradual body weight loss starting on day 5 and splenic histological abnormalities (reduced blue-purple-stained nuclei indicating lymphocyte depletion).
Molecular Weight

461.53

Formula

C26H28FN5O2
CAS No.
SMILES

FC1=CC=C(C(C(N[C@H](C2=CC=C(C=C2)NC(NCC3=CC=CN=C3)=O)C)=O)=C1)N4CCCC4
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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Nampt-IN-17 Related Classifications

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  • 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:

Nampt-IN-173077970-78-3NAMPTApoptosisNicotinamide phosphoribosyl transferasePBEFVisfatinpre-B cell-enhancing factorPre-B cell colony enhancing factororally active NAMPT inhibitordeplete intracellular NAD+ and ATPdisrupt mitochondrial membrane potentialinduce cell cycle arrest and apoptosissuppress cell proliferation invasion and migrationNAPRT-deficient gastric cancerHGC-27 cellsMKN-74 cellsMKN-45 cellsAGS cellsGES-1 cellsBALB/c nude miceSD ratsKM miceInhibitorinhibitorinhibit

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