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Cat. No.: HY-181578

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Nampt-IN-17

Nampt-IN-17 is an selective orally active NAMPT inhibitor with a human NAMPT IC₅₀ of 17 nM and K_i 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.

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

CAS No.: 3077970-78-3
Formula: C₂₆H₂₈FN₅O₂
Molecular Weight:461.53

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (274 KB)

Nampt-IN-17 Chemical Structure

CAS No.: 3077970-78-3

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

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 K_d 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.

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	T_1/2	T_max	C_max	AUC_0-∞	MRT_0-∞	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).

Chemical Information

CAS No. 3077970-78-3
Molecular Weight 461.53
Formula C₂₆H₂₈FN₅O₂
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

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (274 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Yang H, et al. Discovery of Potent o-Aminobenzoamide-Based NAMPT Inhibitors for Targeting NAPRT-Deficient Gastric Cancer. J Med Chem. 2026;69(3):2625-2646. [Content Brief]

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

100 mg

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