Propagermanium
Propagermanium is an orally active and selective CCR2 inhibitor. Propagermanium enhances IFN-γ, IL-2, 2',5'-oligoadenylate synthetase, and unspecified cytokine production, and induces mature cytolytic NK cell subsets. Propagermanium reduces HBe antigen and HBV DNA polymerase levels, promotes HBV clearance and lowers serum ALT. Propagermanium downregulates STAT1, inhibits pro-inflammatory microglia polarization, pro-inflammatory cytokine release, and monocyte/macrophage infiltration. Propagermanium can be used for the research of chronic hepatitis B, atherosclerosis, breast cancer, non-alcoholic steatohepatitis, insulin resistance, refractory gastric cancer, multiple myeloma, type 2 diabetes.
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- CAS No.: 126595-07-1
- Formule: (C6H10Ge2O7)x
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
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CCR2 |
Propagermanium (1-10 μM; 24 h) protects BV2 microglia from OGD/R injury, reduces pro-inflammatory cytokine release and pro-inflammatory marker expression, while leaving anti-inflammatory mediators unchanged[2].
Propagermanium (1-10 μM; 24 h) inhibits LPS-induced pro-inflammatory cytokine release and pro-inflammatory marker expression in BV2 microglia, without affecting anti-inflammatory mediators[2].
Propagermanium (1-10 μM; 24 h) inhibits LPS + IFN-γ-induced pro-inflammatory marker expression and STAT1 phosphorylation in BV2 microglia[2].
Propagermanium (1-10 μM; 24 h) has no significant effect on cytokine release in IL-4-stimulated BV2 microglia[2].
Propagermanium (0.1-10 μg/mL; 15 min pre-incubation) dose-dependently inhibits MCP-1-induced chemotaxis of THP-1 cells, with significant inhibition starting at 0.1 μg/mL[3].
Propagermanium (0.1-1 μg/mL; 15 min pre-incubation) dose-dependently inhibits MCP-1-induced chemotaxis of human PBMC-derived monocytes, with significant inhibition starting at 0.3 μg/mL[3].
Propagermanium (0.1-1 μg/mL; 15 min pre-incubation) dose-dependently inhibits MCP-3-induced chemotaxis of human PBMC-derived monocytes, with significant inhibition starting at 0.1 μg/mL[3].
Propagermanium does not affect intracellular cAMP concentrations in MCP-1-treated THP-1 cells[3].
Propagermanium does not affect MCP-1-induced intracellular Ca2+ mobilization in THP-1 cells[3].
Propagermanium does not inhibit MCP-1 binding to THP-1 cells[3].
Propagermanium (1 μg/mL; 45 min pre-incubation) enhances protein tyrosine phosphorylation at ~80 kDa and ~100 kDa in THP-1 cells independent of MCP-1 treatment[3].
Propagermanium (3 µg/mL; 24 h) potently inhibits MCP-1-stimulated adhesion of J774.1 mouse monocytes to apoE-KO mouse aortic endothelial cells in vitro, with no effect on basal adhesion[5].
Propagermanium (0.1-3 μg/mL; 2 h) concentration-dependently suppresses MCP-1-induced migration of human monocyte THP-1 cells in vitro, with activity observed at clinically relevant concentrations[6].
Propagermanium selectively inhibits MCP-1-induced chemotaxis of CCR2-positive monocytes in vitro[8].
Propagermanium (250 ng/mL-10 μg/mL; 14 days) does not directly induce maturation or activation of isolated NK cells from healthy donors in vitro[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:murine BV2 microglia
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Concentration:1 μM; 3 μM; 10 μM
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Incubation Time:24 h
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Result:Significantly increased BV2 cell survival (P < 0.01) compared to OGD/R-only cells.
Reduced the OGD/R-induced release of pro-inflammatory cytokines IL-6 (P < 0.05, P < 0.01) and TNF-α (P < 0.01), while having no significant effect on anti-inflammatory cytokines IL-10 and TGF-β (P > 0.05).
Downregulated the mRNA expression of pro-inflammatory markers iNOS and CD86 (P < 0.05), without significantly altering the mRNA levels of anti-inflammatory markers Arg1 and CD206 (P > 0.05).
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Cell Line:murine BV2 microglia
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Concentration:1 μM; 3 μM; 10 μM
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Incubation Time:24 h
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Result:Inhibited LPS-induced release of pro-inflammatory cytokines IL-6 (P < 0.05, P < 0.01) and TNF-α (P < 0.01), while having no significant effect on anti-inflammatory cytokines IL-10 and TGF-β (P > 0.05).
Downregulated LPS-induced mRNA overexpression of pro-inflammatory markers iNOS and CD86 (P < 0.05) at concentrations of 3 and 10 μM.
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Cell Line:murine BV2 microglia
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Concentration:1 μM; 3 μM; 10 μM
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Incubation Time:24 h
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Result:Reversed LPS + IFN-γ-induced increases in mRNA expression of pro-inflammatory markers iNOS and CD86 (P < 0.05).
Inhibited LPS + IFN-γ-induced overexpression of p-STAT1 and STAT1 (P < 0.01, P < 0.05).
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Cell Line:murine BV2 microglia
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Concentration:1 μM; 3 μM; 10 μM
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Incubation Time:24 h
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Result:Had no significant effect on IL-4-induced release of anti-inflammatory cytokines IL-10 and TGF-β (P > 0.05), nor did it affect the levels of pro-inflammatory cytokines TNF-α and IL-6 (P > 0.05).
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Cell Line:human monocytic THP-1 cells
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Concentration:0.1-10 μg/mL
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Incubation Time:15 min
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Result:Dose-dependently inhibited MCP-1-induced migration of THP-1 cells, with significant inhibition observed at all tested concentrations (0.1 μg/mL: p < 0.05; 0.3, 1, 3, 10 μg/mL: p < 0.01).
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Cell Line:human peripheral blood mononuclear cell (PBMC)-derived monocytes
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Concentration:0.1-1 μg/mL
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Incubation Time:15 min
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Result:Dose-dependently inhibited MCP-1-induced migration of human PBMC-derived monocytes, with significant inhibition observed at 0.3 μg/mL and 1 μg/mL (p < 0.01).\nDose-dependently inhibited MCP-3-induced migration of human PBMC-derived monocytes, with significant inhibition observed at all tested concentrations (0.1 μg/mL: p < 0.05; 0.3, 1 μg/mL: p < 0.01).
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Cell Line:human monocytic THP-1 cells
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Concentration:1 μg/mL
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Incubation Time:45 min
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Result:Enhanced protein tyrosine phosphorylation at ~80 kDa and ~100 kDa in THP-1 cells, with a 4.6-fold increase compared to nontreated cells; this enhancement occurred regardless of MCP-1 treatment.
| Species | Dose | Route | Plasma Concentration |
|---|---|---|---|
| Rabbit[6] | 9 mg/kg | p.o. | 0.2 μg/mL |
Propagermanium (500-1000 mg/kg; i.p.; daily; several months) does not cause significant weight changes or major organ histologic abnormalities in rats[1].
Propagermanium (125-500 mg/kg; i.v.; daily; 6 months) does not alter body weight gain, body temperature, or heart rate in beagle dogs, with treated animals showing improved biological condition relative to controls[1].
Propagermanium (i.p.; single dose) has an intraperitoneal LD50 of 2.8 g/kg in mice[1].
Propagermanium (25-50 mg/kg/day; p.o.; once every 8 hours; 3 days) protects against ischemic stroke in mice by reducing infarct size, brain edema, and neurologic impairment, inhibiting pro-inflammatory cytokine release and microglia polarization, and downregulating STAT1 phosphorylation[2].
Propagermanium (8 mg/kg; daily; 20 days with standard diet) reduces cortical neuroinflammatory gene expression and astrogliosis, and reduces select cerebellar neuroinflammatory gene expressions, in Hexa-/-Neu3-/- Tay-Sachs disease mice; when given (8 mg/kg; daily; 10 days alongside ketogenic diet), it adds further reductions to cortical Ccl5 and Cxcl10 expression and cerebellar neuroinflammatory markers compared to ketogenic diet alone, but does not reduce cortical macrophage/monocyte intensity or standalone cerebellar macrophage/monocyte or astrocyte intensity[4].
Propagermanium (0.005%; p.o.; daily; 1 week) reduces thioglycollate-induced total inflammatory cell infiltration by ~46% and macrophage infiltration by ~52% in male C57BL/6 mice at 4 days post-injection[5].
Propagermanium (5 mg/kg per day; p.o.; daily; 8 or 12 weeks) reduces aortic root atherosclerotic lesion area by 50% at 8 weeks and 36% at 12 weeks, and reduces macrophage infiltration in lesions by 66% at 8 weeks, in atherogenic diet-fed apoE-KO mice[5].
Propagermanium (9 mg/kg; p.o.; daily; 3 months) significantly suppresses atherosclerotic lesion formation, intimal thickening, and macrophage accumulation in WHHL rabbits without affecting serum lipid profiles[6].
Propagermanium (0.05% w/w; p.o.; 18 weeks (early)/12 weeks (late)) early administration significantly attenuates HFD-induced insulin resistance, WAT inflammation, and NASH development in male C57BL/6J mice, while late administration shows weaker or non-significant effects, except for a reduced hepatic M1/M2 macrophage ratio[8].
Propagermanium (2,400 ppm; p.o.; ad libitum daily; 8 weeks) causes no significant renal toxicity in normal male Wistar rats[10].
Propagermanium (480-2,400 ppm; p.o.; ad libitum daily; 8 weeks) does not exacerbate adriamycin-induced glomerular renal injury in male Wistar rats[10].
Propagermanium (2,400 ppm; p.o.; ad libitum daily; 3 days) does not exert toxic effects on mercuric chloride-induced acute proximal tubular renal injury in male Wistar rats, and tends to reduce associated BUN elevation[10].
Propagermanium (50 mg/kg/day; p.o.; daily; 3 months) improves fasting glucose, insulin resistance, endothelial function, and restores PVAT anticontractile properties in male type 2 diabetic GK rats (both non-high-fat diet and high-fat diet-fed) via anti-inflammatory and antioxidant effects, without altering lipid profiles in non-high-fat diet rats[12].
Propagermanium (0.1-3.0 mg/kg; p.o.; once daily; 4 days) dose-dependently reduces acute liver injury in C. parvum/LPS-treated mice, with significant hepatoprotective activity observed at doses ≥0.3 mg/kg, including a 53% reduction in IFN-γ production at 3.0 mg/kg[13].
Propagermanium (1.0-3.0 mg/kg; p.o.; once daily; 4 days) accelerates antigen-specific immune reaction in C. parvum-primed mice, significantly increasing IFN-γ production by 1.6-fold at 3.0 mg/kg[13].
Propagermanium (1.0-3.0 mg/kg; p.o.) does not influence liver injury in mice treated with LPS alone at doses up to 3.0 mg/kg[13].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 J (male, 22-24 g, middle cerebral artery occlusion for 45 minutes followed by reperfusion)[2]
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Dosage:25 mg/kg/day; 50 mg/kg/day
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Administration:p.o.; once every 8 hours; 3 days
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Result:Significantly reduced infarct size (P < 0.01).
Alleviated brain edema (P < 0.01).
Improved neurologic behavioral impairment (P < 0.05 for 25 mg/kg, P < 0.01 for 50 mg/kg).
Increased relative apparent diffusion coefficient (rADC) at 50 mg/kg dose compared to MCAO controls (P < 0.05).
Blunted the MCAO-induced increase in pro-inflammatory cytokines TNF-α, IFN-γ, IL-1β, IL-6, IL-12, IL-17, and IL-23 (P < 0.01 or P < 0.05).
Had no effect on anti-inflammatory cytokines TGF-β and IL-10.
Downregulated mRNA expression of pro-inflammatory markers iNOS and CD86 (P < 0.05).
Had no effect on anti-inflammatory markers Arg1 and CD206.
Significantly reduced the percentage of CD16+/Iba1+ pro-inflammatory microglia (P < 0.01).
Had no effect on CD206+/Iba1+ anti-inflammatory microglia.
Decreased the ratio of p-STAT1/STAT1 compared to MCAO controls (P < 0.05 for 25 mg/kg, P < 0.01 for 50 mg/kg).
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Animal Model:Hexa-/-Neu3-/- (Tay-Sachs disease model, genetically engineered with GM2 ganglioside accumulation-induced neuroinflammation)[4]
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Dosage:8 mg/kg
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Administration:daily; 10 or 20 days
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Result:Reduced cortical neuroinflammation-related gene expression ratios: Ccl2 from ~0.0013 to ~0.0003, Ccl3 from ~0.006 to ~0.003, Ccl5 from ~0.0022 to ~0.0008, Cxcl10 from ~0.004 to ~0.002, and Gfap from ~0.38 to ~0.17.
Reduced cortical GFAP-positive astrocyte intensity from ~25,000 to ~15,000.
Did not significantly reduce cortical MOMA-2-positive macrophage/monocyte intensity (~33,000 in untreated mice).
Reduced cerebellar neuroinflammatory gene expression ratios: Ccl2 from ~0.0022 to ~0.0003, Ccl3 from ~0.0055 to ~0.0032, and Gfap from ~0.25 to ~0.22.
Did not significantly reduce cerebellar GFAP-positive astrocyte intensity (~40,000 in untreated mice) or MOMA-2-positive macrophage/monocyte intensity (~43,000 in untreated mice).
Further reduced cortical Ccl5 and Cxcl10 expression compared to ketogenic diet alone.
Reduced cerebellar GFAP-positive astrocyte intensity from ~40,000 to ~27,000.
Reduced cerebellar MOMA-2-positive macrophage/monocyte intensity compared to untreated mice.
Did not alter anxiety-related behavior in the open field test or neuromotor activity in the rotarod test compared to untreated mice.
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Animal Model:C57BL/6 (male)[5]
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Dosage:0.005%
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Administration:p.o.; daily; 1 week
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Result:Reduced total infiltrated cells to 1466 ×10000 cells at 4 days post-thioglycollate injection.
Reduced macrophage counts to 1082 ×10000 cells at 4 days post-thioglycollate injection.
Did not affect granulocyte or lymphocyte counts at either 1 day or 4 days post-injection.
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Animal Model:apoE-KO (male, female; backcrossed onto C57BL/6 background; weaned at 4 weeks, fed atherogenic high cholesterol diet)[5]
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Dosage:0.005%; 5 mg/kg per day
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Administration:p.o.; daily; 8 or 12 weeks
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Result:Reduced aortic root atherosclerotic lesion area to 0.62 mm2 (50% reduction) after 8 weeks on diet.
Reduced macrophage-positive lesion area to 0.23 mm2 (66% reduction) after 8 weeks on diet.
Reduced percentage of macrophage-positive area relative to total lesion area to 36.1% (32% reduction) after 8 weeks on diet.
Reduced aortic root lesion area to 1.36 mm2 (36% reduction) after 12 weeks on diet.
Reduced descending thoracic aorta atherosclerotic lesion coverage to 6.2% (37% reduction) after 12 weeks on diet.
Did not affect plasma lipid levels, MCP-1 levels, body weight, or T lymphocyte infiltration in lesions.
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Animal Model:WHHL (2.5-month-old, 2.7 kg, genetically lacking LDL receptors)[6]
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Dosage:9 mg/kg
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Administration:p.o.; daily; 3 months
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Result:Did not alter serum lipid profiles (total cholesterol, LDL, HDL, triglyceride, lipid peroxides) compared to baseline or controls.
Significantly suppressed the oil red O-positive atherosclerotic lesion area in the aortic arch, thoracic aorta, and total aorta (p < 0.05), and tended to suppress lesions in the abdominal aorta.
Significantly suppressed maximal intimal thickness in the aortic arch, abdominal aorta, and total aorta (p < 0.05 or p < 0.01).
Significantly suppressed intimal area in the abdominal aorta and total aorta (p < 0.05 or p < 0.01).
Significantly suppressed RAM11-positive macrophage accumulation in the aortic arch, thoracic aorta, and abdominal aorta (p < 0.05 or p < 0.01).
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Animal Model:C57BL/6J (male, 9-week-old at study start, acclimatized to 12 weeks old before diet initiation, HFD-induced NASH)[8]
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Dosage:0.05% w/w
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Administration:p.o.; 18 weeks (early intervention); 12 weeks (late intervention)
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Result:Significantly reduced fasting plasma insulin levels, C-peptide levels, and HOMA-IR compared to HFD controls (early intervention only).
Significantly increased plasma adiponectin levels compared to HFD controls (early intervention only).
Significantly reduced WAT gene expression of pro-inflammatory markers Mcp-1 and CD11c compared to HFD controls (early intervention only); late intervention showed non-significant trend toward reduced CD11c expression.
Significantly reduced hepatic macrovesicular steatosis by 37% compared to HFD controls (early intervention only); late intervention showed non-significant 31% reduction.
Showed borderline significant reduction (p=0.05) in hepatic lobular inflammatory cell aggregates compared to HFD controls (early intervention only).
Significantly reduced hepatic M1/M2 macrophage ratio (CD11c/Arginase-1 expression) compared to HFD controls (both early and late interventions).
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Animal Model:Wistar (male, 7 weeks old after 1 week acclimation)[10]
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Dosage:2,400 ppm
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Administration:p.o.; ad libitum daily; 8 weeks
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Result:Showed very slight basophilic changes of tubules in one rat (also present in a control rat).
Showed basophilic change in distal tubular epithelium, tubular dilatation, interstitial mononuclear cell infiltration, urinary casts, and hemorrhage in a second rat.
Had no renal lesions in all other rats.
Observed no significant renal toxic effects overall.
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Animal Model:Wistar (male, 7 weeks old after 1 week acclimation, adriamycin-induced glomerular damage)[10]
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Dosage:480 ppm; 2,400 ppm
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Administration:p.o.; ad libitum daily; 8 weeks
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Result:Caused no alterations to renal changes observed in adriamycin-only control rats, including light microscopic findings (hyalin droplets in podocytes, basophilic changes of tubules, urinary casts, tubular dilatation, focal and segmental glomerular sclerosis, interstitial mononuclear cell infiltration, hemorrhage) and ultrastructural findings (swelling of glomerular podocytes, partial fusion of foot processes, electron dense droplets/vacuoles in podocytes, proximal tubular changes like decreased cell organelles, flattened epithelium, thickened basal lamina).
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Animal Model:Wistar (male, 7 weeks old after 1 week acclimation, mercuric chloride-induced proximal tubular damage)[10]
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Dosage:2,400 ppm
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Administration:p.o.; ad libitum daily; 3 days
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Result:Showed histopathological changes (basophilic changes of tubules, mitosis of tubular epithelium, desquamation of tubular epithelium, urinary casts, tubular dilatation, dilatation of interstitial capillaries at end of treatment; basophilic changes, urinary casts, tubular dilatation, mononuclear cell infiltration after recovery) similar in incidence and grade to mercuric chloride-only control rats.
Tended to reduce BUN elevation from 65 mg/dL in controls to 46 mg/dL, though this change was not statistically significant.
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Animal Model:Goto-Kakizaki (GK) (male, initial mean body weight 294 g, 8 months old at study endpoint; spontaneous type 2 diabetes model; separate arm fed high-fat diet for 5 months to induce metabolic impairment)[12]
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Dosage:50 mg/kg/day
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Administration:p.o.; daily; 3 months
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Result:Reduced fasting glucose levels by 18% (p < 0.01) in non-high-fat diet GK rats.
Reduced insulin resistance by 32% (p < 0.05) in non-high-fat diet GK rats.
Improved endothelial-dependent relaxation in aortas without PVAT by 23% (from 52.6% to 75.6%, p < 0.05) and with PVAT by 33% (from 34.04% to 72.5%, p < 0.05) in non-high-fat diet GK rats.
Reduced PVAT inflammation by 56% (p < 0.05) and oxidative stress by 55% (p < 0.05) in non-high-fat diet GK rats.
Reduced PVAT CD36 levels to ~140% of non-high-fat diet GK control (p < 0.05) in non-high-fat diet GK rats.
Reduced PVAT nitrotyrosine levels to ~140% of non-high-fat diet GK control (p < 0.05) in non-high-fat diet GK rats.
Reduced serum alanine aminotransferase (ALT) levels in non-high-fat diet GK rats.
Improved vascular sensitivity to sodium nitroprusside (SNP) in non-high-fat diet GK rats.
Reduced fasting glucose levels to 81.5 mg/dL (p < 0.01 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Reduced triglyceride levels by 18% (p < 0.05 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Increased total cholesterol levels by 22% (p < 0.01 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Reduced insulin resistance (p < 0.05 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Improved endothelial-dependent relaxation in aortas without PVAT and with PVAT (p < 0.001 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Reduced PVAT inflammation and oxidative stress in high-fat diet-fed GK rats.
Reduced PVAT CD36 levels to ~170% of high-fat diet GK control (p < 0.05 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Reduced PVAT nitrotyrosine levels to ~190% of high-fat diet GK control (p < 0.05 vs. high-fat diet GK controls) in high-fat diet-fed GK rats.
Reduced serum ALT and alkaline phosphatase (ALP) levels in high-fat diet-fed GK rats.
Improved vascular sensitivity to SNP in high-fat diet-fed GK rats.
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Animal Model:ICR mice (female, 7 weeks old, acute liver injury induced by i.v. heat-killed Corynebacterium parvum followed by i.v. lipopolysaccharide)[13]
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Dosage:0.1 mg/kg; 0.3 mg/kg; 1.0 mg/kg; 3.0 mg/kg
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Administration:p.o.; once daily; 4 days
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Result:Reduced serum AST and ALT levels to 38% of control values (AST: P < 0.001, ALT: P < 0.01 versus control), significantly inhibited hepatocellular necrosis, and reduced liver infiltration of mononuclear cells at 1.0 mg/kg.
Caused significant attenuation of serum ALT and AST activity, reduced IFN-γ production, and prevented infiltration of CD4- and CD11b-positive cells into the liver at 0.3 mg/kg.
Reduced IFN-γ production by 53% (P < 0.05 versus control), significantly inhibited IL-12 production (reduced by 51% at 3 hours and 58% at 4 hours versus control), prevented infiltration of CD4- and CD11b-positive cells into the liver, and reduced liver mononuclear cell infiltration and hepatocellular necrosis at 3.0 mg/kg.
Reduced TNF-α production by 20% and IL-1α production by 28% (not statistically significant) at 3.0 mg/kg.
Resulted in only 1 mouse with severe liver injury (grade 4) at 1.0 mg/kg, compared to 7 mice in the control group (P < 0.05 versus control).
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Animal Model:ICR mice (female, 7 weeks old, Corynebacterium parvum immune primed by i.v. heat-killed C. parvum)[13]
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Dosage:1.0 mg/kg; 3.0 mg/kg
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Administration:p.o.; once daily; 4 days
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Result:Significantly augmented serum IFN-γ concentration to 1.6 times that of C. parvum-primed control mice (P < 0.05 versus control) at 3.0 mg/kg.
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Animal Model:ICR mice (female, 7 weeks old, LPS-induced liver injury by i.v. lipopolysaccharide)[13]
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Dosage:1.0 mg/kg; 3.0 mg/kg
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Administration:p.o.
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Result:Did not alter serum AST levels compared to LPS-only control mice.
Chemical Information
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CAS No. 126595-07-1
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Formule (C6H10Ge2O7)x
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SMILES
O=[Ge](CCC(O)=O)O[Ge](CCC(O)=O)=O.[n]
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Hirayama C, et al. Propagermanium: a nonspecific immune modulator for chronic hepatitis B. J Gastroenterol. 2003;38(6):525-532. [Content Brief]
[2]. He S, et al. Propagermanium, a CCR2 inhibitor, attenuates cerebral ischemia/reperfusion injury through inhibiting inflammatory response induced by microglia. Neurochem Int. 2019;125:99-110. [Content Brief]
[3]. Yokochi S, et al. An anti-inflammatory drug, propagermanium, may target GPI-anchored proteins associated with an MCP-1 receptor, CCR2. J Interferon Cytokine Res. 2001;21(6):389-398. [Content Brief]
[4]. Inci OK, et al. Combined treatment of Ketogenic diet and propagermanium reduces neuroinflammation in Tay-Sachs disease mouse model. Metab Brain Dis. 2025;40(3):133. Published 2025 Feb 28. [Content Brief]
[5]. Yamashita T, et al. Propagermanium reduces atherosclerosis in apolipoprotein E knockout mice via inhibition of macrophage infiltration. Arterioscler Thromb Vasc Biol. 2002;22(6):969-974. [Content Brief]
[6]. Eto Y, et al. Long-term treatment with propagermanium suppresses atherosclerosis in WHHL rabbits. J Cardiovasc Pharmacol. 2003;41(2):171-177. [Content Brief]
[7]. Masuda T, et al. Phase I dose-escalation trial to repurpose propagermanium, an oral CCL2 inhibitor, in patients with breast cancer. Cancer Sci. 2020;111(3):924-931. [Content Brief]
[8]. Mulder P, et al. The CCR2 Inhibitor Propagermanium Attenuates Diet-Induced Insulin Resistance, Adipose Tissue Inflammation and Non-Alcoholic Steatohepatitis. PLoS One. 2017;12(1):e0169740. Published 2017 Jan 11. [Content Brief]
[9]. Kikuchi S, et al. Propagermanium Induces NK Cell Maturation and Tends to Prolong Overall Survival of Patients With Refractory Cancer. Anticancer Res. 2019;39(9):4687-4698. [Content Brief]
[10]. Asano K, et al. Influence of propagermanium (SK-818) on chemically induced renal lesions in rats. J Toxicol Sci. 1994;19 Suppl 2:131-143. [Content Brief]
[11]. Tsutsumi Y, et al. Effectiveness of propagermanium treatment in multiple myeloma patients. Eur J Haematol. 2004;73(6):397-401. [Content Brief]
[12]. Azul L, et al. Propagermanium as a Novel Therapeutic Approach for the Treatment of Endothelial Dysfunction in Type 2 Diabetes. Int J Mol Sci. 2024;25(15):8328. Published 2024 Jul 30. [Content Brief]
[13]. Yokochi S, et al. Hepatoprotective effect of propagermanium on Corynebacterium parvum and lipopolysaccharide-induced liver injury in mice. Scand J Immunol. 1998;48(2):183-191. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Propagermanium Related Classifications
HY-19009B Related Classifications
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