dorsomorphin (Compound C)

Pre-administration of AM-630 (selective CB2R antagonist; 0.5 and 1 mg/kg;i.p.) and BML-275 i.e. AMP activated protein kinase (AMPK) mediated autophagy inhibitor; 1.5 and 3 mg/kg;i.p.) substantially abrogated the cardioprotective response of RIPC. The current findings highlight the pivotal role of CB2R activation and AMPK activated autophagy in cardioprotective mechanism of RIPC against MIRI.

Meanwhile, AMPK inhibitor Dorsomorphin overturned the protective effect of GLS2 downregulation on myocardial cells. GLS2 silencing repressed myocardial damage in vivo. SP1-activated GLS2 could aggravate H/R-induced cardiomyocyte injury and ferroptosis by inactivating the AMPK/mTOR pathway, providing a promising therapeutic target for MIRI treatment in the future.

Myocardial ischemia-reperfusion injury (MIRI) causes severe clinical complications in patients. Further analysis showed that GEM administration prevented the I/R-induced decrease in phospho-AMPK levels in ischemic cardiac tissue, and pharmacological inhibition of AMPK with dorsomorphin (DSMF) abolished all cardioprotective effects of GEM. Taken together, these results suggest that GEM mitigates MIRI-induced cardiac injury by inhibiting apoptosis and oxidative stress via modulation of AMPK, supporting its potential for reducing MIRI-related cardiac damage.

This was confirmed by pathway inhibitors (Dorsomorphin, ESI-09) and siRNA knockdown, which reversed cell cycle arrest and reduced cytotoxicity...Crucially, AMPK inhibition attenuated Ad-VT's antitumor effects. These results demonstrate that Ad-VT exerts potent, tumor-selective activity against bladder cancer by inducing cAMP-dependent AMPK-Raptor-mTOR signaling and G2/M arrest, supporting its therapeutic potential.

Specifically, AdipoRon preferentially suppressed ACC1 expression and subsequently downregulated CPT1A, indicating disruption of fatty acid metabolism. These findings establish that AdipoRon suppresses MM progression through AMPK-driven metabolic reprogramming and apoptosis induction, positioning adiponectin receptor agonism as a promising therapeutic strategy for multiple myeloma.

These changes were consistent with AMPK activation, and pharmacological inhibition of AMPK with dorsomorphin (compound C) abolished cytokine production in VPS34-IN1-treated cells. Together, these results indicate that differential cytokine responses to autophagy inhibition are driven primarily by metabolic rewiring rather than autophagic flux per se, highlighting the interplay between metabolism, mitochondrial ROS, and signaling pathways in pDC activation.

Interestingly, dorsomorphin inhibited the expression and nucleation of Gli1 and Gli3 but not affected the expression of Gli2. Thus, these findings reveal that the new mechanism of AMPK inhibitor dorsomorphin against prostate cancer metastasis is through synergistically antagonizing JAK2/STAT3 and Gli2-independent Shh activation.

CC abolished all DIM-induced molecular changes in vitro. Collectively, DIM alleviates hepatic lipid accumulation and oxidative stress in MASLD models through AMPK activation, subsequently modulating PPARα and SREBP1/ACC1 pathways.

Furthermore, administration of Compound C, an AMPK inhibitor, reversed the suppressive effects of CLDN1 knockdown on cell proliferation, EMT, and lipid metabolism, indicating the AMPK signaling pathway is involved in CLDN1-mediated EMT and lipid metabolism in CRC cells. These findings suggest that CLDN1 plays a significant role in EMT and lipid metabolism of CRC cells and can be utilized as a therapeutic target for CRC.

Fibrate drug FNF exerts antitumor effects by targeting the mitochondrial complex I-AMPK/mTOR-CD276 axis, inducing mitochondrial dysfunction, and downregulating the immunosuppressive molecule CD276 to activate T cell-mediated antitumor immunity. This study provides a potential strategy for drug repurposing and identifies a novel target for immunotherapeutic combination strategies in bladder cancer.

These findings suggest that AM-1241 PostC exerts cardioprotective effects in MIRI through modulation of inflammatory, fibrosis, apoptotic and AMPK-mediated autophagy pathways.

Moreover, treatment with an AMPK inhibitor (dorsomorphin) suppressed CAIX-induced HSPA6 expression and the metastasis of U2OS cells. In conclusion, the results indicate that CAIX overexpression mediates HSPA6 expression through the AMPK signalling pathway, which consequently induces the metastasis of OS cells.