In vivo, oral administration of YM-1 at 1 mM for 7 days demonstrated therapeutic effects in Drosophila models of polyglutamine (polyQ) toxicity, attributed to the activation of Hsp70. This outcome highlights YM-1's potential for treating neurodegenerative diseases by enhancing the protective functions of molecular chaperones^[1].

YM-1 also influences the maturation process of neuronal nitric oxide synthase (nNOS) by facilitating Hsp70-dependent steps and partially inhibiting the formation of the ATP-bound form of nNOS. Moreover, YM-1 enhances the interaction between Hsp70 and its unfolded substrates, showcasing its role in protein folding processes^[1].

At concentrations ranging from 0 to 200 μM, YM-1 activates Hsp70 binding to its substrates, and between 0.001 to 1000 μM, it shifts Hsp70 into its high-affinity conformation for substrates, displaying an IC50 value of 8.2 μM for binding efficacy to Hsp70. This transition suggests YM-1's capability to modulate Hsp70's substrate affinity and function^[1].

YM-1 has been observed to promote the ubiquitination of nNOS at concentrations from 0.1 to 1 μM after 24 hours, indicating a role in regulating nNOS stability and signaling^[1].

When applied to cell cultures at 5 and 10 μM for 24 to 48 hours, it not only induces cell death in HeLa cells but also causes growth arrest in hTERT-RPE1 cells, reflecting its differential effects on cancerous and non-cancerous cells^[2].

Notably, a concentration of 10 μM for 48 hours leads to the upregulation of tumor suppressor proteins p53 and p21, while downregulating the oncogenic proteins FoxM1 and survivin, suggesting a potential therapeutic role in cancer treatment through modulation of these critical cellular pathways^[2].