| Features: |
| Psoralidin is a prenylated coumestan isolated primarily from Psoralea corylifolia (Babchi). It is not a classical anticancer drug. Psoralidin generally acts to suppress oncogenic signaling and survival pathways while promoting apoptosis in tumor cells. Reported effects (context-dependent, preclinical): -DOWNREGULATES pro-survival pathways (e.g., NF-κB, STAT3) -UPREGULATES apoptotic signaling (caspase activation) -MODULATES androgen receptor signaling in prostate cancer models -SENSITIZES tumor cells to chemo- and radio-induced stress This positions psoralidin as a biologic modulator, not a driver. Across cancer cell and animal models, psoralidin has been associated with: -Apoptosis induction -Caspase activation -Mitochondrial depolarization -Inflammatory pathway suppression -NF-κB inhibition -STAT3 attenuation -Hormone signaling modulation -Androgen receptor suppression (prostate cancer context) -Oxidative stress interaction -Redox imbalance tipping tumor cells toward death under stress Psoralidin is best described as chemopreventive or chemo-sensitizing, not chemoprotective |
| Source: |
| Type: |
| Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases.
S, G1, G2, and M are the four phases of mitosis. |
| 4967- | PSO, | Psoralidin's Anti-Cancer Mechanisms: A Technical Guide |
| - | Review, | Var, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:389 Target#:322 State#:% Dir#:2
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