AMPK

BML-275 is a cell-permeable pyrazolopyrimidine compound shown to be an AMP-activated protein kinase (AMPK) and fatty acid synthase inhibitor.

Dorsomorphin, also known as BML-275, is a selective small molecule inhibitor of BMP signaling, which promotes cardiomyogenesis in embryonic stem cells. Dorsomorphin reverses the mesenchymal phenotype of breast cancer initiating cells by inhibition of bone morphogenetic protein signaling.

WZ4003 is a highly specific NUAK kinase inhibitor with IC50 of 20 nM and 100 nM for NUAK1 and NUAK2

ETC-1002 is a novel, first-in-class, orally available, once-daily LDL-C lowering small molecule; activator of hepatic AMP-activated protein kinase (AMPK); also has potent inhibitory activity against hepatic ATP-citrate lyase(IC50=29 uM).

HTH-01-015 is a potent and selective inhibitor of NUAK1 (IC50 = 100 nM) and does not affect the activity of a panel of 139 other kinases, including additional AMPK family members.

MARK-IN-2 is a potent microtubule affinity regulating kinase (MARK) inhibitor with an IC50 of 5 nM.

MARK-IN-1 is a potent microtubule affinity regulating kinase (MARK) inhibitor with an IC50 of <0.25 nM.

STO-609 is a selective and cell-permeable inhibitor of the Ca2+/calmodulin-dependent protein kinase kinase (CaM-KK), with Ki values of 80 and 15 ng/mL for recombinant CaM-KKα and CaM-KKβ, respectively.

Urolithin B is one of the gut microbial metabolites of ellagitannins, and has anti-inflammatory and antioxidant effects. Urolithin B is also a regulator of skeletal muscle mass.

EB-3D is a potent and selective choline kinase α (ChoKα) inhibitor, with an IC50 of 1 μM for ChoKα1.

Marein is a natural compound with multifaceted pharmacological properties, including HDAC inhibition with an IC₅₀ of 100 μM. It exerts neuroprotective effects by preserving mitochondrial function and activating the AMPK signaling pathway. In HepG2 cells, Marein improves high glucose–induced insulin resistance by enhancing glucose uptake via the CaMKK/AMPK/GLUT1 pathway, promoting glycogen synthesis through the IRS/Akt/GSK-3β pathway, and suppressing gluconeogenesis via the Akt/FoxO1 axis. Additionally, Marein possesses antioxidative, antihypertensive, antihyperlipidemic, and antidiabetic properties, making it a promising candidate for metabolic and neurodegenerative disease research.

SU212 acts as an ENO1 inhibitor and AMPK activator, selectively inducing oxidative phosphorylation while reducing glycolysis and glucose uptake in tumor cells. This compound binds directly to ENO1, promoting apoptosis and ENO1 degradation through proteasomal and autophagic pathways, without affecting normal cells. Additionally, SU212 leads to mitotic arrest and apoptosis in triple-negative breast cancer (TNBC) cells, showcasing significant anti-tumor activity in vitro. It inhibits tumor growth and metastasis in various in vivo models, including syngeneic, xenograft, and diabetic mice, and has demonstrated an excellent safety profile, making it a valuable tool for research in TNBC, diabetes, and fatty liver disease.

Panduratin A is a potent inhibitor of the NF-κB signaling pathway, recognized for its significant anti-inflammatory and antioxidant properties. It demonstrates protective effects against nephrotoxicity induced by Colistin, primarily by mitigating oxidative stress and enhancing mitochondrial function. Additionally, Panduratin A activates autophagy through an AMPK-dependent mechanism and exhibits potential anti-tuberculosis and antiviral activities by inhibiting the methyltransferase of SARS-CoV-2. These diverse biological activities make Panduratin A a valuable tool in various areas of research, including inflammation, cellular stress responses, and infectious diseases.

MRT199665 is a potent, ATP-competitive inhibitor targeting MARK, SIK, and AMPK pathways, exhibiting IC50 values of 2 nM for MARK1, 10 nM for AMPKα1, and 110 nM for SIK1. This compound induces apoptosis in MEF2C-activated human acute myeloid leukemia (AML) cells by effectively inhibiting the phosphorylation of the SIK substrate CRTC3 at S370. MRT199665 serves as a valuable tool for investigating the roles of MARK, SIK, and AMPK in cellular signaling and cancer biology.

OSU-53 is an orally active AMPK activator and a direct mTOR inhibitor, exhibiting an EC50 of 0.3 μM. This compound induces autophagy by facilitating the conversion of LC3 I to LC3 II and plays a crucial role in modulating energy homeostasis by downregulating fatty acid biosynthesis while enhancing oxidative metabolism through upregulation of PGC1α and NRF-1. OSU-53 demonstrates antitumor activity across various cancer models, including breast and thyroid cancers, making it a valuable tool for cancer research and metabolic studies.

AMPK activator 16 is a potent AMP-activated protein kinase (AMPK) activator that effectively enhances AMPK signaling. It promotes the phosphorylation of AMPK, subsequently increasing the levels of phosphorylated acetyl-CoA carboxylase (p-ACC) and phosphorylated raptor (p-raptor) in N2a cells. This compound is instrumental in studies exploring metabolic regulation and signaling pathways linked to energy homeostasis and cellular stress responses.

BAY-3827 is a potent and selective inhibitor of AMP-activated protein kinase (AMPK), exhibiting IC50 values of 1.4 nM at low ATP concentrations (10 μM) and 15 nM at higher ATP concentrations (2 mM). This compound demonstrates over 500-fold selectivity against a wide array of kinases, making it a valuable tool for elucidating AMPK-related pathways. BAY-3827 effectively inhibits the phosphorylation of acetyl-CoA carboxylase 1 and displays significant anti-proliferative effects in androgen-dependent prostate cancer cell lines, supporting its application in cancer research and metabolic studies.

AMPK-IN-3 is a potent and selective inhibitor of AMP-activated protein kinase (AMPK), exhibiting IC50 values of 60.7 nM for AMPK α2, 107 nM for AMPK α1, and 3820 nM for KDR. This compound effectively inhibits AMPK without impacting cell viability or inducing significant cytotoxicity in K562 cells. AMPK-IN-3 is valuable for research focused on cancer biology and the role of AMPK in metabolic regulation and cellular energy homeostasis.

Chromium(III) acetate functions as an AMPK inhibitor by inhibiting the phosphorylation of AMP-activated protein kinase (AMPK), subsequently promoting lipogenesis. This compound exhibits low toxicity in mammalian models, demonstrated by an LD50 of 2365 mg/kg in rats. It is primarily utilized in research to explore metabolic pathways and the regulation of energy homeostasis.

AMPK-IN-4 is a selective inhibitor of AMP-activated protein kinase (AMPK), targeting both AMPKα1 and AMPKα2 with IC50 values of 393 nM and 141 nM, respectively. This compound is significant in cancer research, facilitating investigations into metabolic regulation and cellular energy homeostasis. Its efficacy in modulating AMPK activity makes it a valuable tool for studying the pathways associated with tumor metabolism and potential therapeutic strategies.

AMPK/mTOR modulator-1 is a Ginsenoside derivative functioning as both an mTOR inhibitor and AMPK activator. It activates AMPK signaling with a Kd of 4.759 μM, promoting M1-like tumor-associated macrophage polarization while inhibiting M2-like polarization. This compound enhances glycolysis and demonstrates significant anti-inflammatory activity alongside inhibition of tumor progression. AMPK/mTOR modulator-1 is ideal for research focused on colorectal cancer and related metabolic disorders.

NUAK1-IN-3 is a selective inhibitor of NUAK1 with a high potency, exhibiting an IC50 of 0.49 nM. It also demonstrates inhibitory activity against NUAK2 and JAK3 with IC50 values of 265 nM and 225 nM, respectively. This compound disrupts the NUAK1-MYPT1 signaling pathway, leading to reduced MYPT1 phosphorylation and inhibition of proliferation, migration, and invasion in triple-negative breast cancer cells. Additionally, NUAK1-IN-3 counteracts TGF-β1-induced epithelial-mesenchymal transition effects by modulating critical markers such as Snail, N-cadherin, and E-cadherin. It holds potential for exploring therapeutic strategies for triple-negative breast cancer.