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| Berbamine — berbamine is a natural bisbenzylisoquinoline alkaloid with pleiotropic anticancer signaling activity. It is best classified as a plant-derived small-molecule natural product and investigational anticancer lead rather than an approved oncology drug. Standard abbreviation: BBM. It is chiefly isolated from Berberis species, especially Berberis amurensis, and has also been reported in other alkaloid-containing medicinal plants. The strongest mechanistic signal in cancer appears to be inhibition of CaMKIIγ-centered survival signaling, with downstream effects on c-Myc, STAT3, β-catenin, PI3K/Akt-related survival programs, apoptosis, and in some models ROS-linked stress responses. Clinical oncology translation remains limited; most evidence is preclinical, and formulation constraints have been noted because native berbamine has limited tumor-site exposure and short plasma persistence in vivo. Primary mechanisms (ranked):
Bioavailability / PK relevance: Native berbamine appears PK-limited for systemic oncology use. Multiple papers describe short plasma half-life or poor tumor-site exposure as a practical limitation, which is one reason nanoparticle and derivative strategies have been pursued. I did not find a robust modern human PK package for parent berbamine suitable for quantitative clinical extrapolation; stronger PK data were easier to find for derivatives than for the native compound. In-vitro vs systemic exposure relevance: Many mechanistic cancer studies use micromolar in-vitro concentrations, often around 5–20 μM and sometimes higher. That makes direct translation to achievable free systemic exposure uncertain for native berbamine. Mechanistic direction is plausible, but potency-to-exposure matching remains a major translational bottleneck unless formulation or structural optimization is used. Clinical evidence status: Preclinical for cancer. Evidence includes cell culture and xenograft studies across leukemia and several solid tumors, plus medicinal-chemistry optimization work on derivatives. I did not find established randomized oncology trials or standard clinical deployment for cancer treatment. Berbamine is a bisbenzylisoquinoline alkaloid, meaning it is composed of two benzylisoquinoline moieties. Its unique structure distinguishes it from many other natural alkaloids Berbamine is most often isolated from the plant Berberis, commonly known as barberry. Various species within this genus have been used in traditional Chinese medicine and other herbal traditions. plants in genera like Stephania have also been reported to contain bisbenzylisoquinoline alkaloids like berbamine. These plants are used in various parts of Asia both for their stimulant effects and other medicinal purposes.Oxidative Stress: Berbamine can increase the production of reactive oxygen species within cancer cells. Elevated ROS levels may push cancer cells beyond their threshold of tolerance, leading to oxidative stress–induced cell death. This property also ties in with its ability to modulate apoptosis and autophagy. Berbamine is a promising natural compound with multifaceted anticancer properties. Its ability to induce apoptosis, cause cell cycle arrest, modulate key signal transduction pathways (such as JAK/STAT, NF-κB, and PI3K/Akt/mTOR), and affect autophagy, makes it a candidate for further investigation in various cancer models. A calcium channel blocker. Mechanistic relevance in cancer
P: 0–30 min |
| Source: HalifaxProj(inhibit) CGL-CS TCGA |
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| Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses. Anti-inflammatory cytokine. In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling. - In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis. In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β. - TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion. Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses. Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers. - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment. High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types. |
| 5536- | BBM, | Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers |
| - | 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
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