Ramucirumab (CYRAMZA) / angioG Cancer Research Results

Ramu, Ramucirumab (CYRAMZA): Click to Expand ⟱

Features:

Ramucirumab (CYRAMZA) is a fully human IgG1 monoclonal antibody that binds VEGFR-2 (KDR/Flk-1) on endothelial cells and blocks VEGF-A/VEGF-C/VEGF-D from activating the receptor, thereby suppressing VEGFR-2 phosphorylation and downstream pro-angiogenic signaling (endothelial proliferation, migration, survival, and vascular permeability). Clinically, it’s used as an anti-angiogenic therapy across multiple solid tumors (labelled indications include advanced/metastatic gastric/GEJ adenocarcinoma, NSCLC in specific combinations/settings, metastatic colorectal cancer in combination therapy, and AFP-high hepatocellular carcinoma after prior therapy).

Pathways/axes ramucirumab functionally down-modulates (via VEGFR-2 blockade)
-VEGF ligand → VEGFR-2 angiogenesis axis (core target): vessel sprouting, endothelial survival, migration, permeability.
-PI3K → AKT (PKB) survival signaling downstream of VEGFR-2 (endothelial cell survival/anti-apoptosis).
-RAS → RAF → MEK → ERK (MAPK) proliferation signaling downstream of VEGFR-2 (endothelial proliferation).
-PLCγ → PKC signaling downstream of VEGFR-2 (linked to permeability and other endothelial responses).
-Src-family kinases / TSAd–Src modules and FAK/integrin–cytoskeleton signaling (migration, adhesion, barrier regulation).
-eNOS → nitric oxide (NO) signaling (vascular tone/permeability; intersects with Src and PLCγ signaling). -Vascular permeability & “vascular normalization” effects that can secondarily modulate tumor hypoxia/HIF programs and immune cell trafficking/antitumor immunity in the microenvironment (context-dependent).

angioG, angiogenesis: Click to Expand ⟱

Source:

Type:

Process through which new blood vessels.
Angiogenesis, the process of new blood vessel formation from pre-existing vessels, plays a crucial role in cancer progression and metastasis. Tumors require a blood supply to grow beyond a certain size and to spread to other parts of the body.
Vascular Endothelial Growth Factor (VEGF): VEGF is one of the most important pro-angiogenic factors. It stimulates endothelial cell proliferation and migration, leading to the formation of new blood vessels. Many tumors overexpress VEGF, which correlates with poor prognosis.
Hypoxia-Inducible Factor (HIF): In response to low oxygen levels (hypoxia), tumors can activate HIF, which in turn promotes the expression of VEGF and other angiogenic factors. This mechanism allows tumors to adapt to their microenvironment and sustain growth.

Scientific Papers found: Click to Expand⟱

5284-

Ramu,

https://pmc.ncbi.nlm.nih.gov/articles/PMC4131847/

Review,

Var,

VEGFR2↓, OS↑, angioG↓, toxicity↝, ChemoSen↑, Dose↝,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:

Angiogenesis & Vasculature ⓘ

angioG↓, 1, VEGFR2↓, 1,

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1, Dose↝, 1,

Functional Outcomes ⓘ

OS↑, 1, toxicity↝, 1,
Total Targets: 6

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: angioG, angiogenesis

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