Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema[1][2][3][4].
细胞效力 (Cellular Effect)
Cell Line
Type
Value
Description
References
BV-2
IC50
> 10 μM
Compound: 25
Antiinflammatory activity in C57BL6/J mouse BV2 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay
Antiinflammatory activity in C57BL6/J mouse BV2 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay
Antiviral activity against Influenza A virus (A/Vietnam/1194/2004(H5N1)) infected in MDCK cells assessed as inhibition of viral replication after 2 to 3 days by crystal violet staining-based plaque reduction assay
Antiviral activity against Influenza A virus (A/Vietnam/1194/2004(H5N1)) infected in MDCK cells assessed as inhibition of viral replication after 2 to 3 days by crystal violet staining-based plaque reduction assay
KYSE 170 and EC109 esophageal squamous cell carcinoma cells
Concentration:
50 μg/mL
Incubation Time:
24 h, 36 h, 72 h
Result:
Induced S-phase cell cycle arrest, mitochondrial membrane permeabilization, and caspase-dependent apoptosis in KYSE 170 and EC109 cells. Upregulated autophagy- and apoptosis-related proteins, including NDRG1, BNIP3, and Beclin, with significant reduction in cell viability by 50-70% compared to controls.
MC3T3-E1 preosteoblasts and RAW264.7 monocyte cells
Concentration:
5 mg/mL (MC3T3-E1); 1-4 mg/mL (RAW264.7)
Incubation Time:
3-14 days (MC3T3-E1); 6 days (RAW264.7)
Result:
In MC3T3-E1 cells, significantly increased alkaline phosphatase (ALP) activity (2-fold at day 10), collagen type I deposition (1.5-fold at day 14), and mineralized nodule formation (34% increase at week 5).
In RAW264.7 cells, at 2-4 mg/mL dose-dependently reduced TRAP-positive multinucleated osteoclast formation by 54-77% and decreased TRAP enzyme activity, indicating inhibition of osteoclast differentiation.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Subcutaneous bone tissue engineering model (Balb/c nude mice) (6 weeks old), subcutaneous transplantation of alginate-encapsulated hMSCs[3]
Dosage:
5 mg/bead or 50 mg/bead, incorporated into alginate gel
Administration:
Single subcutaneous injection into the back, observed for 5-8 weeks
Result:
Promoted osteogenic differentiation of human mesenchymal stem cells (hMSCs), as shown by von Kossa and Alizarin Red staining for calcium deposition.
Increased expression of collagen type I and osteocalcin in the transplanted tissue, with dose-dependent enhancement (50 mg/bead showing stronger effects).
Resulted organized new bone formation with reduced fibrous tissue compared to control groups.
Intraperitoneal injection, daily for 3 days, followed by 30-min coronary artery occlusion and 120-min reperfusion
Result:
Significantly reduced infarct size by 68% compared to controls, associated with increased nitric oxide (NO) production, activation of mitochondrial ATP-sensitive potassium (mitoKATP) channels, and downregulation of nuclear factor-κB (NF-κB)-dependent pro-inflammatory cytokines (TNF-α, IL-6). Western blot analysis showed upregulation of hypoxia-inducible factor-1α (HIF-1α) and heme oxygenase-1 (HO-1), while immunohistochemistry revealed reduced neutrophil infiltration in the ischemic myocardium.
Animal Model:
Acute hypobaric hypoxia model (Sprague-Dawley rats) (180±20 g), acute hypobaric hypoxia at 9144 m for 5 h[4]
Dosage:
75 mg/kg, dissolved in DMSO/saline
Administration:
Intraperitoneal injection, daily for 3 days prior to hypoxia exposure
Result:
Reduced brain water content (edema index) by 10% and vascular permeability (sodium fluorescein leakage) by 49% compared to hypoxic controls. Decreased levels of pro-inflammatory cytokines (TNF-α, IL-6, IFN-γ) and increased anti-inflammatory IL-10. Upregulated HIF-1α, HO-1, and metallothionein-1 (MT-1) expression, while NF-κB nuclear translocation and vascular cell adhesion molecule-1 (VCAM-1) expression were significantly attenuated.
*请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (stored under nitrogen)。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。
可选溶剂
浓度溶剂体积质量
1 mg
5 mg
10 mg
25 mg
DMSO
1 mM
5.4892 mL
27.4461 mL
54.8923 mL
137.2307 mL
5 mM
1.0978 mL
5.4892 mL
10.9785 mL
27.4461 mL
10 mM
0.5489 mL
2.7446 mL
5.4892 mL
13.7231 mL
15 mM
0.3659 mL
1.8297 mL
3.6595 mL
9.1487 mL
20 mM
0.2745 mL
1.3723 mL
2.7446 mL
6.8615 mL
25 mM
0.2196 mL
1.0978 mL
2.1957 mL
5.4892 mL
30 mM
0.1830 mL
0.9149 mL
1.8297 mL
4.5744 mL
40 mM
0.1372 mL
0.6862 mL
1.3723 mL
3.4308 mL
50 mM
0.1098 mL
0.5489 mL
1.0978 mL
2.7446 mL
60 mM
0.0915 mL
0.4574 mL
0.9149 mL
2.2872 mL
80 mM
0.0686 mL
0.3431 mL
0.6862 mL
1.7154 mL
100 mM
0.0549 mL
0.2745 mL
0.5489 mL
1.3723 mL
Help & FAQs
Do most proteins show cross-species activity?
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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