DL-Propargylglycine hydrochloride
Based on 2 publication(s) in Google Scholar
DL-Propargylglycine hydrochloride is an irreversible and selective CSE inhibitor that blocks the biosynthesis of endogenous hydrogen sulfide. DL-Propargylglycine hydrochloride induces ROS and TGF-β1 expression. DL-Propargylglycine hydrochloride downregulates carotid ACE2 and Ang-(1-7), and elevates Ang II. DL-Propargylglycine hydrochloride upregulates ICAM-1/LFA-1, exacerbating Aspirin (HY-14654)-induced gastric mucosal injury. DL-Propargylglycine hydrochloride is used in research on diabetes-induced liver injury, diabetic nephropathy, atherosclerosis, gastric mucosal injury, hemorrhagic shock, and Streptococcus agalactiae infection.
For research use only. We do not sell to patients.
- CAS No.: 16900-57-5
- Formula: C5H8ClNO2
- Molecular Weight:149.58
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) DL-Propargylglycine hydrochloride
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Biological Activity
Description
IC50 & Target
[2]|
ACE2 |
In Vitro
DL-Propargylglycine (48 h) hydrochloride significantly increases the proliferation of HBZY-1 rat mesangial cells, mimicking the effect of high glucose[2].
DL-Propargylglycine hydrochloride significantly increases TGF-β1 mRNA levels in HBZY-1 rat mesangial cells[2].
DL-Propargylglycine (0.3 mM; 12 h) hydrochloride attenuates melatonin-induced improvement of growth and photosynthetic parameters in Triticum aestivum L. cv. Pandas under drought stress[4].
DL-Propargylglycine (0.3 mM; 12 h) hydrochloride attenuates the melatonin-induced improvement of relative water content and soluble protein levels in Triticum aestivum L. cv. Pandas under drought stress[4].
DL-Propargylglycine (0.3 mM; 12 h) hydrochloride inhibits L-DES activity and reduces endogenous H2S levels in Triticum aestivum L. cv. Pandas under drought stress[4].
DL-Propargylglycine (0.3 mM; 12 h) hydrochloride reduces melatonin-induced improvement of glyoxalase system activity in Triticum aestivum L. cv. Pandas under drought stress[4].
DL-Propargylglycine (2 mM; 5 min) hydrochloride inhibits H2S production in rat gastric mucosal homogenates[5].
DL-Propargylglycine hydrochloride slightly increases PFK activity in AR-GBS[8].
DL-Propargylglycine hydrochloride enhances ROS generation in HBZY-1 rat mesangial cells, mimicking the effects of high glucose[2].
DL-Propargylglycine (0.3 mM; 12 h) hydrochloride attenuates the melatonin-induced reduction of oxidative stress markers in Triticum aestivum L. cv. Pandas under drought stress[4].
DL-Propargylglycine (0.3 mM; 12 h) hydrochloride reduces melatonin-induced enhancement of antioxidant enzyme activity in Triticum aestivum L. cv. Pandas under drought stress[4].
DL-Propargylglycine hydrochloride alters bacterial metabolism and cell wall/membrane structure in Streptococcus agalactiae[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
DL-Propargylglycine (30 mg/kg; injection; single dose) hydrochloride exerts limited synergistic effects in the AR-GBS-infected zebrafish model[8].
DL-Propargylglycine (25 mg/kg; intravenous injection; single injection; 15 min after morphine) hydrochloride enhances the ability of L-CYSee to overcome morphine-induced ventilatory depression, in which the effects of the first dose of L-CYSee on TV, MV, EEP, PIF, PEF, EF50, and ExpD are enhanced, and the effects of the second dose of L-CYSee on Freq, TV, MV, PIF, PEF, EF50, InspD, and ExpD are more significantly enhanced[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J male apoE−/− (8 weeks old)[3]
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Dosage:10 mg/kg/day
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Administration:i.p.; daily; 4 weeks
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Result:Induced advanced atherosclerosis with more severe neointimal hyperplasia and more obvious narrowness in LCA.
Enhanced hyperplasia of collagen fibers in neointimal lesions.
Had negligible effect on body weight, plasma lipid profiles, and blood pressure.
Inhibited the expression of ACE2 in endothelial cells in atherosclerotic lesions.
Downregulated carotid ACE2 expression.
Inhibited the local production of Ang-(1-7) in LCA and raised the carotid level of Ang II.
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Animal Model:Zebrafish (average length 2.5-3 cm, average weight 0.2 g)[8]
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Dosage:30 mg/kg
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Administration:single dose; 1 hour post-infection
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Result:Induced 80% mortality rate in combination with ampicillin.
Did not enhance efficacy when bacteria were pretreated for 6 h prior to infection.
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Animal Model:Sprague Dawley (adult male, 395-396 g body weight)[9]
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Dosage:25 mg/kg
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Administration:i.v.; single injection; 15 min after morphine
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Result:Augmented L-CYSee-induced changes in TV, MV, EEP, PIF, PEF, EF50, and ExpD after the first L-CYSee dose.
More markedly augmented L-CYSee-induced changes in Freq, TV, MV, PIF, PEF, EF50, InspD, and ExpD after the second L-CYSee dose.
Increased changes in TV, MV, PIF, PEF, inspiratory drive, and expiratory drive during hypoxic-hypercapnic gas challenge.
Increased changes in TV, MV, PIF, PEF, EF50, inspiratory drive, and expiratory drive upon return to room-air.
Did not produce an increase in EEP upon return to room-air, unlike vehicle-treated rats.
Total morphine-induced changes from baseline were similar to vehicle-treated rats, including TV (-13%), MV (-16%), Ti (+43%), EIP (+109%), PIF (-25%), EF50 (+62%), relaxation time (-29%), apneic pause (+29%), inspiratory drive (-40%), and NEBI (-54%).
Chemical Information
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CAS No. 16900-57-5
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Molecular Weight 149.58
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Formula C5H8ClNO2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (2)
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Journal Impact Factor
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Most Recent
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- DL-Propargylglycine
- 16900-57-5
- Reactive Oxygen Species (ROS)
- TGF-β Receptor
- Angiotensin-converting Enzyme (ACE)
- Integrin
- pyridoxal 5'-phosphate site
- L-DES activity
- AR-GBS
- mesangial cell proliferation
- HBZY-1 rat mesangial cells
- Streptococcus agalactiae
- CSE inhibitor
- hydrogen sulfide biosynthesis
- Triticum aestivum L. cv. Pandas
- 3-MST inhibitor
- Inhibitor
- inhibitor
- inhibit