NAMPT

CHS-828 is a potent inhibitor of NAD+ biosynthesis enzyme NAMPT with IC50 <25 nM.

GNE-617 is a potent nicotinamide phosphoribosyltransferase (NAMPT) inhibitor with IC50 value of 5nM.

STF 118804 is a highly specific NAMPT inhibitor that reduces the viability of most B-ALL cell lines with high potency IC50 values in the low nanomolar range and improves survival in an orthotopic xenotransplant model of high-risk acute lymphoblastic leukemia.

KPT 9274 ( ATG-019) is an orally bioavailable small molecule that is a non-competitive dual inhibitor of PAK4 and NAMPT. It shows an IC50 of ~120 nM for NAMPT in a cell-free enzymatic assay.

Nampt-IN-3 (Compound 35) simultaneously inhibit nicotinamide phosphoribosyltransferase (NAMPT) and HDAC with IC50s of 31 nM and 55 nM, respectively. Nampt-IN-3 effectively induces cell apoptosis and autophagy and ultimately leads to cell death.

LB-60-OF61 is a NAMPT inhibitor and is a cytotoxic compound with a selectivity towards MYC overexpressing cell lines.

CB30865(ZM 242421) is a potent inhibitor of Nampt , an enzyme present in the NAD biosynthetic pathway.

Nampt-IN-1 (LSN3154567) is a potent and selective NAMPT inhibitor. Nampt-IN-1 inhibits purified NAMPT with an IC50 of 3.1 nM.

BRD4/NAMPT-IN-1 (Compound A2) is a dual inhibitor of NAMPT and BRD4, with IC₅₀ values of 35 nM and 58 nM, respectively. It suppresses the growth and migration of hepatocellular carcinoma cells and induces apoptosis. In the HCCLM3 xenograft mouse model, BRD4/NAMPT-IN-1 exhibits potent anticancer activity without apparent toxicity.

OT-82 is a selective, orally active inhibitor of Nicotinamide Adenine Dinucleotide Phosphate (NAMPT). It exhibits potent cytotoxicity specifically towards hematopoietic cells and induces cell death in a NAD+ dependent manner. Due to these properties, OT-82 shows potential as an innovative antineoplastic agent for investigating hematological malignancies.

HDAC/NAMPT-IN-1 is a potent dual inhibitor of histone deacetylases (HDAC) and nicotinamide adenine dinucleotide (NAD+) biosynthesis enzyme NAMPT, exhibiting IC50 values ranging from 0.72 to 37081 nM for HDAC and 1618 nM for NAMPT. This compound demonstrates significant potential in modulating cellular acetylation levels and metabolic processes associated with cancer and neurodegenerative diseases. Its application in research can facilitate studies on epigenetic regulation and NAD+ metabolism, contributing to a deeper understanding of cellular mechanisms and therapeutic strategies.

(E/Z)-Daporinad hydrochloride is a potent inhibitor of nicotinamide phosphoribose transferase (NAMPT). By specifically targeting NAMPT, this compound induces apoptosis through the gradual depletion of intracellular NAD+. (E/Z)-Daporinad hydrochloride is utilized in research to explore mechanisms in cancer biology and inflammatory diseases.

PDEδ/NAMPT IN-1 is a potent dual inhibitor targeting phosphodiesterase 6 (PDE6) with a binding affinity of 0.410 nM and nicotinamide phosphoribosyl transferase (NAMPT) with an IC50 of 2.21 nM. This compound effectively disrupts KRAS-related signaling pathways and hampers the synthesis of nicotinamide adenine dinucleotide (NAD+), leading to apoptosis in KRAS mutant pancreatic cancer cells. PDEδ/NAMPT IN-1 holds significant potential for advancing research in KRAS mutant pancreatic cancer.

Daporinad hydrochloride is a potent non-competitive inhibitor of nicotinamide phosphoribosyltransferase (Nampt), with a Ki of 0.3 nM. It induces cellular effects such as depletion of NAD+ and ATP levels, suppression of the mTORC1 and MAPK/ERK signaling pathways, and activation of TFEB, leading to enhanced autophagy. Additionally, Daporinad hydrochloride disrupts the endoplasmic reticulum calcium pool, impairing T cell activation through diminished mitogen-induced calcium signaling. This compound is valuable for research in myeloma, liver cancer, and immunosuppression, with effects including cell cycle arrest and apoptosis in various cancer cell lines.

Nampt-IN-8 is a selective inhibitor of Nicotinamide Adenine Dinucleotide Phosphate (NAMPT) with an IC50 value of 0.183 μM. This compound effectively induces apoptosis in cultured cells and enhances reactive oxygen species (ROS) production. It is a valuable tool for research on metabolic regulation and cellular stress responses, particularly in studies related to cancer and neurodegenerative diseases.

PARP1/NAMPT-IN-2 is a potent dual inhibitor of PARP1 and NAMPT, exhibiting IC50 values of 0.8 nM and 18 nM, respectively. This compound effectively inhibits cell proliferation and migration, while inducing apoptosis in breast cancer cells. PARP1/NAMPT-IN-2 is particularly relevant for investigating therapeutic strategies in triple-negative breast cancer research.

CHS-828 (nicotinate) is a competitive inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), exhibiting an IC50 of less than 25 nM. This compound effectively reduces cellular levels of NAD+, leading to cytotoxic effects on cancer cells. CHS-828 is primarily utilized in cancer research applications, studying its anti-tumor properties and mechanisms of action in various malignancies.

Mutant IDH1/NAMPT-IN-1 is a dual inhibitor targeting mutant isocitrate dehydrogenase 1 (mutant IDH1) and nicotinamide phosphoribosyltransferase (NAMPT), with IC50 values of 14.93 nM and 12.56 nM, respectively. This compound effectively induces apoptosis, making it a valuable tool for research into cancer mechanisms and treatment strategies. Additionally, Mutant IDH1/NAMPT-IN-1 demonstrates the capability to cross the blood-brain barrier, enhancing its potential for applications in neurological studies and therapies.

Nampt-IN-16 is a potent NAMPT inhibitor exhibiting an IC50 value of 0.15 μM. This compound effectively reduces intracellular levels of NAD+ and ATP, leading to the inhibition of proliferation, migration, and invasion in gastric cancer cells. Additionally, Nampt-IN-16 induces cell cycle arrest and apoptosis while altering cellular metabolism. It is a valuable tool for research focused on tumors, particularly gastric cancer.

PARP1/NAMPT-IN-1 is a potent dual inhibitor of PARP1 and NAMPT, exhibiting IC50 values of 1.2 nM and 6.7 nM, respectively. This compound disrupts the homologous recombination repair pathway, leading to the accumulation of DNA double-strand breaks, which induces cell cycle arrest and apoptosis. Additionally, PARP1/NAMPT-IN-1 demonstrates antimigratory effects and has shown significant antitumor activity in a breast cancer xenograft model. It is a valuable tool for research on triple-negative breast cancer (TNBC).

PD-L1/Nampt-IN-1 is a dual inhibitor targeting PD-L1 and NAMPT (nicotinamide phosphoribosyltransferase) with IC50 values of 63 nM and 582 nM, respectively. This compound exhibits cross-species affinity with comparable KD values for human PD-L1 (52.6 nM) and mouse PD-L1 (49.1 nM). PD-L1/Nampt-IN-1 facilitates tumor growth inhibition by enhancing the tumor immune microenvironment, making it a valuable tool for research in melanoma studies.

GPP78 is a potent inhibitor of nicotinamide adenine dinucleotide (NAD) biosynthesis via the enzyme Nampt, demonstrating an IC50 of 3.0 nM. It exhibits cytotoxicity in the neuroblastoma SH-SY5Y cell line, with an IC50 of 3.8 nM, primarily by inducing autophagy. GPP78 serves as a valuable tool in cancer and inflammatory research, highlighting its potential therapeutic applications in oncology.

Nampt-IN-10 is a potent inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), exhibiting nanomolar inhibitory activity in various cancer cell lines, including MDA-MB453, NCI-N87, and NCI-H526. This compound can be utilized as a payload in antibody-drug conjugates (ADCs), where it has been shown to enhance anti-tumor efficacy. It serves as a valuable tool for researchers investigating NAMPT's role in cancer metabolism and therapeutic resistance.

Nampt-IN-5 is a potent inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), a crucial enzyme in the NAD+ biosynthesis pathway. It demonstrates significant biological activity with cellular IC50 values of 0.7 nM against A2780 cells and 3.9 nM against COR-L23 cells, indicating strong efficacy in targeting cancer metabolism. In addition, Nampt-IN-5 inhibits CYP3A4 activity, making it relevant for studies on drug metabolism and potential interactions. Research applications include cancer cell metabolism and the investigation of therapeutic strategies targeting NAD+ pathways.

NAMPT/IDO1-IN-1 is a dual inhibitor of NAMPT and IDO1, exhibiting IC50 values of 57.7 nM and 233 nM, respectively. By inhibiting NAMPT, this compound interferes with NAD+ biosynthesis, thereby suppressing the proliferation and migration of drug-resistant NSCLC cell lines, such as A549/R. Additionally, NAMPT/IDO1-IN-1 demonstrates significant antitumor activity in vivo and enhances the sensitivity of these resistant cells to paclitaxel treatment. This compound is valuable for research in cancer biology and the development of therapeutic strategies aimed at overcoming drug resistance.

Nampt-IN-10 TFA is a potent inhibitor of Nicotinamide Phosphoribosyltransferase (NAMPT). It exhibits significant cellular potency against A2780 and CORL23 cell lines, with IC50 values of 5 nM and 19 nM, respectively. This compound serves as a promising non-antimitotic payload for antibody-drug conjugates (ADCs) in cancer research, highlighting its potential in therapeutic applications targeting NAMPT-related metabolic pathways.

Nampt-IN-15 is an inhibitor of nicotinamide adenine dinucleotide (NAD) biosynthesis through the inhibition of nicotinamide phosphoribosyltransferase (Nampt). It exhibits potent cytotoxicity in various cancer cell lines, including BxPC-3, HepG2, L540cy, and MOLM-13, with IC50 values of 38.5 nM, 8 nM, 8.5 nM, and 7 nM, respectively. This compound is valuable for research applications focused on cancer metabolism and therapeutic strategies targeting NAMPT in tumor cells.

GNE-618 is a potent inhibitor of nicotinamide phosphoribosyl transferase (NAMPT) with an IC50 of 6 nM. By depleting cellular NAD levels, GNE-618 induces apoptosis in tumor cells, exhibiting significant anti-tumor activity. This compound is primarily applied in cancer research, facilitating the study of NAD metabolism and its implications in oncology.

GNE-617 hydrochloride is a potent inhibitor of NAMPT (Nicotinamide adenine dinucleotide biosynthesis regulator) with an IC50 of 5 nM. This compound effectively disrupts NAMPT enzymatic activity, leading to decreased levels of NAD+ in cellular systems. GNE-617 has demonstrated significant efficacy in various xenograft cancer models, making it a valuable tool for investigating cancer metabolism and the therapeutic potential of targeting NAD+ synthesis.

A-1293201 is a potent NAMPT inhibitor that demonstrates antitumor activity by reducing total cellular NAD+/NADH levels. This reduction leads to significant ATP depletion, ultimately resulting in the induction of cancer cell death. Additionally, A-1293201 effectively addresses the acquired resistance mechanism associated with the NAMPT Y18 mutant, providing a promising avenue for research in cancer treatment.

LB-60-OF61 hydrochloride is a potent inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), demonstrating significant cytotoxic effects. This compound shows selective activity against MYC-overexpressing cell lines, making it a valuable tool in cancer research. Its specific targeting of NAMPT allows for investigations into pathways related to cellular metabolism and cancer cell survival.

Nampt-IN-9 is a potent inhibitor of nicotinamide adenine dinucleotide (NAD+) biosynthesis via the enzyme NAMPT. It exhibits significant anticancer activity and has potential applications in research focusing on pancreatic ductal adenocarcinoma. This compound serves as a valuable tool for studying the metabolic pathways and therapeutic strategies related to cancer treatment.

Nampt-IN-13 is a selective inhibitor of nicotinamide adenine dinucleotide (NAD+) biosynthesis through the inhibition of nicotinamide phosphoribosyltransferase (NAMPT). This compound demonstrates significant anti-proliferative effects and is utilized in the study of tumor metabolism and cancer therapy. Its application is particularly relevant in the synthesis of antibody-drug conjugates (ADCs) for targeted cancer treatment research.

MS7 is a potent inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), which is often overexpressed in cancer cells to sustain NAD+ levels necessary for rapid cell proliferation. By targeting NAMPT, MS7 serves as a valuable tool for developing PROTAC A7, an effective degrader of NAMPT. This reagent holds significant potential for research applications in cancer biology, particularly in studies focused on metabolic regulation and therapeutic strategies targeting NAMPT.

Nampt-IN-7 is a potent inhibitor of nicotinamide adenine dinucleotide (NAD+) biosynthesis by targeting NAMPT, with an IC50 of 7.31 μM. This compound exhibits significant cytotoxicity against the HepG2 hepatocellular carcinoma cell line, demonstrated by an IC50 of 24.28 μM. Nampt-IN-7 is valuable for research applications focusing on cancer metabolism and therapeutic strategies targeting NAD+ synthesis in tumor cells.

AS1604498 is a selective competitive inhibitor of human nicotinamide adenine dinucleotide (NAD) biosynthesis enzyme NAMPT, demonstrating an IC50 of 44.4 nM. By inhibiting NAMPT activity, AS1604498 effectively reduces the production of nicotinamide mononucleotide and lowers intracellular NAD levels, leading to the activation of caspase 3/7 and the subsequent induction of apoptosis in cancer cells. This compound is particularly relevant for research focused on chronic myeloid leukemia and related metabolic pathways.

Nampt-IN-17 is a selective inhibitor of nicotinamide adenine dinucleotide (NAD+) biosynthesis, targeting NAMPT with an IC50 of 17 nM and a Ki of 25.9 nM in human cells. This compound effectively depletes intracellular NAD+ and ATP levels, leading to disrupted mitochondrial membrane potential and subsequently inhibiting cell proliferation, self-renewal, invasion, and migration. Additionally, Nampt-IN-17 induces cell cycle arrest and apoptosis, demonstrating potent selectivity against NAPRT-deficient gastric cancer cells. It serves as a valuable tool for studying the mechanisms underlying NAPRT-deficient gastric cancer.