2. Membrane Transporter/Ion Channel Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Neuronal Signaling Apoptosis Autophagy
  3. Ferroptosis Autophagy Reactive Oxygen Species (ROS) Sodium Channel Mitophagy NOD-like Receptor (NLR) Glutathione Peroxidase Apoptosis PINK1/Parkin ATP Synthase
  4. Dexpramipexole dihydrochloride

Dexpramipexole dihydrochloride  (Synonyms: (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride)

Cat. No.: HY-17355A Purity: 99.94%
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Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

For research use only. We do not sell to patients.

CAS No. : 104632-27-1

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Based on 2 publication(s) in Google Scholar

Other Forms of Dexpramipexole dihydrochloride:

Dexpramipexole dihydrochloride Related Antibodies

Top Publications Citing Use of Products

    Dexpramipexole dihydrochloride purchased from MedChemExpress. Usage Cited in: Neuroreport. 2023 Mar 1;34(4):220-231.  [Abstract]

    Dexpramipexole (DPX; 3 mg/kg; i.p.; once daily for 6 consecutive days) attenuates the LPS-induced increase in the number of TUNEL-positive cells in the hippocampus in SAE mice.

    Dexpramipexole dihydrochloride purchased from MedChemExpress. Usage Cited in: Neuroreport. 2023 Mar 1;34(4):220-231.  [Abstract]

    Dexpramipexole (DPX; 3 mg/kg; i.p.; once daily for 6 consecutive days) attenuates LPS-induced activation of microglia and astrocytes in the hippocampus in SAE mice. (a) Representative images of Iba-1 staining and quantification of Iba-1 (green) fluorescence intensity in the hippocampal CA1 and DG regions. (b) Representative images of GFAP staining and quantification of GFAP (red) fluorescence intensity in the hippocampal CA1 and DG regions. DAPI staining is shown in blue.

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    NLRP3 NLRP1 NOD1 NOD2

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    GPX1 GPX4

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    Description

    Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more[1][2][3][4][5][6].

    In Vitro

    Dexpramipexole (5-200 μM; 24 h) dihydrochloride shows no cytotoxicity to primary cardiomyocytes isolated from neonatal rats at concentrations below 100 μM, while the compound at 200 μM reduces cell viability[1].
    Dexpramipexole (2-50 μM) dihydrochloride protects primary neonatal rat cardiomyocytes against hypoxia/reoxygenation (H/R)-induced injury by enhancing cell viability and reducing LDH release[1].
    Dexpramipexole (2-50 μM) dihydrochloride upregulates the expression level of PINK1 protein in primary cardiomyocytes from neonatal rats treated with H/R[1].
    Dexpramipexole dihydrochloride protects primary cardiomyocytes from neonatal rats against H/R-induced mitochondrial dysfunction by reducing mPTP opening, decreasing ROS production and restoring mitochondrial membrane potential[1].
    Dexpramipexole dihydrochloride enhances ATG7-dependent mitophagy in primary neonatal rat cardiomyocytes subjected to H/R, which is characterized by increased formation of mitophagosomes, enhanced autophagic mitochondrial sequestration, and improved mitochondrial clearance[1].
    Dexpramipexole dihydrochloride activates PINK1 and Parkin and promotes mitochondrial fission in primary neonatal rat cardiomyocytes exposed to H/R[1].
    Dexpramipexole dihydrochloride protects primary cardiomyocytes from neonatal rats against H/R injury by upregulating PINK1- and Parkin-dependent mitophagy[1].
    Dexpramipexole (10 μM; 5 min) dihydrochloride inhibits tetrodotoxin-resistant sodium currents in primary cultured rat dorsal root ganglion neurons with an IC50 of 294.4 nM, and does not alter the voltage-dependent activation or inactivation properties of the channels[5].
    Dexpramipexole (10 μM) dihydrochloride selectively inhibits Nav1.8-mediated sodium currents in primary cultured dorsal root ganglion neurons from wild-type mice[5].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Dexpramipexole dihydrochloride Related Antibodies
    In Vivo

    Dexpramipexole (1 mg/kg; single administration) dihydrochloride alleviates myocardial ischemia/reperfusion injury in male C57BL/6 mice by reducing infarct size, restoring cardiac function, decreasing serum levels of myocardial injury biomarkers, and enhancing PINK1/Parkin-dependent mitophagy[1].
    Dexpramipexole (5-20 mg/kg; i.p., once daily for 14 consecutive days) dihydrochloride improves survival rate, body weight gain, spontaneous activity, motor coordination and forelimb muscle strength, reduces hematoma volume, alleviates white matter injury, decreases iron and ROS accumulation, and inhibits ferroptosis by upregulating GPX4 and FSP1 in mice with intracerebral hemorrhage[2].
    Dexpramipexole (3 mg/kg; i.p.; once daily for 6 consecutive days) dihydrochloride improves lipopolysaccharide (LPS)-induced cognitive impairment in sepsis-associated encephalopathy (SAE), preserves the morphology and function of hippocampal mitochondria in mice, and inhibits mitochondria-mediated pyroptosis and apoptosis[3].
    Dexpramipexole (3-20 mg/kg; 20-140 μg/20 μL; p.o.; i.p.; hind paw s.c.; single administration) dihydrochloride exerts effective analgesic effects in various mouse models of nociceptive pain (e.g., inflammatory pain, visceral pain) and neuropathic pain (e.g., chemotherapy-induced pain, nerve compression pain, diabetic neuropathic pain)[5].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: C57BL/6 (male, 9-10 weeks old, 24-26 g; intracerebral hemorrhage induced by stereotactic injection of autologous tail vein blood)[2]
    Dosage: 5 mg/kg; 10 mg/kg; 20 mg/kg
    Administration: i.p., once daily for 14 days
    Result: Significantly increased the survival rate of mice after cerebral hemorrhage.
    Slowed down the postoperative weight loss and promoted the recovery of motor function, motor coordination ability, muscle strength and comprehensive neurological function (BMS).
    Reduced iron deposition around the hematoma and the accumulation of reactive oxygen species.
    Increased the expression of GPX4 and FSP1.
    Animal Model: C57BL/6 (male, 3 months old, 20-28 g, LPS-induced sepsis-associated encephalopathy)[3]
    Dosage: 3 mg/kg
    Administration: i.p., once daily for 6 days
    Result: Improved the long-term cognitive dysfunction caused by LPS, particularly spatial working memory and hippocampus-dependent memory.
    Protected the mitochondria of hippocampal neurons, improved their morphology (reduced swelling) and function (maintained ATP levels, reduced ROS).
    Inhibited pyroptosis and apoptosis of cells
    Animal Model: CD-1 (male, 20-25 g, intraplantar formalin injection-induced inflammatory pain)[5]
    Dosage: 3 mg/kg; 10 mg/kg; 20 μg/20 μL; 70 μg/20 μL; 140 μg/20 μL
    Administration: p.o.; single dose 1 h before test; i.p.; single dose 1 h before test; s.c. in hind paw; single dose 10 min before test
    Result: Reduced time spent in pain-like behaviors during the early formalin phase (10 mg/kg p.o.).
    Reduced time spent in pain-like behaviors dose-dependently during the late formalin phase (3 mg/kg, 10 mg/kg p.o.).
    Reduced time spent in pain-like behaviors dose-dependently during the late formalin phase (3 mg/kg, 10 mg/kg i.p.).
    Reduced time spent in pain-like behaviors during the late formalin phase (70 μg/20 μL, 140 μg/20 μL s.c.).
    Caused no effect on pain-like behaviors in the early phase at any tested subdermal dose.
    Animal Model: CD-1 (male, 20-25 g; female, intraperitoneal acetic acid injection-induced visceral pain)[5]
    Dosage: 10 mg/kg; 20 mg/kg
    Administration: i.p.; single dose 1 h before test
    Result: Reduced the number of abdominal writhings dose-dependently in male mice
    . Reduced the number of abdominal writhings in female mice.
    Animal Model: CD-1 (male, 20-25 g, ankle complete Freund adjuvant injection-induced chronic inflammatory arthritis pain)[5]
    Dosage: 70 μg/20 μL
    Administration: s.c. in hind paw; single dose 10 min before each test on day 7, 14, 21
    Result: Increased mechanical thresholds at day 7, 14, and 21 post CFA injection.
    Animal Model: CD-1 (subcutaneous oxaliplatin injection-induced acute chemotherapy-induced neuropathic pain)[5]
    Dosage: 10 mg/kg; 70 μg/20 μL
    Administration: i.p.; single dose 30 min post oxaliplatin; s.c. in hind paw; single dose 50 min post oxaliplatin
    Result: Reduced cold pain-related behaviors at 1, 2, 3, 4, and 5 h post oxaliplatin injection (10 mg/kg i.p.).
    Reduced cold pain-related behaviors at 1 hour post oxaliplatin injection (70 μg/20 μL, s.c.).
    Animal Model: CD-1 (intraperitoneal oxaliplatin injection-induced chronic chemotherapy-induced neuropathic pain)[5]
    Dosage: 10 mg/kg
    Administration: i.p.; single dose 1 h before test; p.o.; single dose 1 h before test
    Result: Reduced cold allodynia at day 21 post initial oxaliplatin injection (10 mg/kg i.p.).
    Reduced cold allodynia at 1, 3, and 6 hours post dosing, with effects diminishing by 9 hours (10 mg/kg p.o.).
    Animal Model: CD-1 (male, 20-25 g, chronic constriction injury of right sciatic nerve-induced neuropathic pain)[5]
    Dosage: 10 mg/kg
    Administration: i.p.; single dose 1 h before test
    Result: Reduced mechanical allodynia in the injured hind paw.
    Animal Model: CD-1 (intraperitoneal streptozotocin injection-induced diabetic neuropathic pain, blood glucose > 250 mg/dl confirmed 3 weeks post-injection)[5]
    Dosage: 10 mg/kg
    Administration: i.p.; single dose 1 h before test
    Result: Increased latency to pain-related behaviors in diabetic mice.
    Clinical Trial
    Molecular Weight

    284.26

    Formula

    C10H19Cl2N3S
    CAS No.
    Appearance

    Solid

    Color

    White to off-white

    SMILES

    NC(S1)=NC2=C1C[C@H](NCCC)CC2.[H]Cl.[H]Cl
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    4°C, sealed storage, away from moisture

    *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 100 mg/mL (351.79 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

    H2O : 100 mg/mL (351.79 mM; Need ultrasonic)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 3.5179 mL 17.5895 mL 35.1791 mL
    5 mM 0.7036 mL 3.5179 mL 7.0358 mL
    View the Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

    * Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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    • Dilution Calculator

    Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

    This equation is commonly abbreviated as: C1V1 = C2V2

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    In Vivo:

    Select the appropriate dissolution method based on your experimental animal and administration route.

    For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
    To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
    The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

    • Protocol 1

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: ≥ 2.08 mg/mL (7.32 mM); Clear solution

      This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

      Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
    • Protocol 2

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

      Solubility: ≥ 2.08 mg/mL (7.32 mM); Clear solution

      This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

      Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

      Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.

    For the following dissolution methods, please prepare the working solution directly. It is recommended to prepare fresh solutions and use them promptly within a short period of time.
    The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

    • Protocol 1

      Add each solvent one by one:  PBS

      Solubility: 100 mg/mL (351.79 mM); Clear solution; Need ultrasonic

    In Vivo Dissolution Calculator
    Please enter the basic information of animal experiments:

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    Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
    Calculation results:
    Working solution concentration: mg/mL
    This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
    The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).
    Purity & Documentation

    Purity: 99.94%

    SDS (396 KB)

    COA (246 KB) LCMS (94 KB)

    Handling Instructions (2659 KB)
    References

    Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

    Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
    DMSO / H2O 1 mM 3.5179 mL 17.5895 mL 35.1791 mL 87.9477 mL
    5 mM 0.7036 mL 3.5179 mL 7.0358 mL 17.5895 mL
    10 mM 0.3518 mL 1.7590 mL 3.5179 mL 8.7948 mL
    15 mM 0.2345 mL 1.1726 mL 2.3453 mL 5.8632 mL
    20 mM 0.1759 mL 0.8795 mL 1.7590 mL 4.3974 mL
    25 mM 0.1407 mL 0.7036 mL 1.4072 mL 3.5179 mL
    30 mM 0.1173 mL 0.5863 mL 1.1726 mL 2.9316 mL
    40 mM 0.0879 mL 0.4397 mL 0.8795 mL 2.1987 mL
    50 mM 0.0704 mL 0.3518 mL 0.7036 mL 1.7590 mL
    60 mM 0.0586 mL 0.2932 mL 0.5863 mL 1.4658 mL
    80 mM 0.0440 mL 0.2199 mL 0.4397 mL 1.0993 mL
    100 mM 0.0352 mL 0.1759 mL 0.3518 mL 0.8795 mL

    * Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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    Dexpramipexole dihydrochloride Related Classifications

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    • 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.

    Keywords:

    Dexpramipexole104632-27-1(R)-PramipexoleR-(+)-PramipexoleKNS-760704KNS760704KNS 760704FerroptosisAutophagyReactive Oxygen Species (ROS)Sodium ChannelMitophagyNOD-like Receptor (NLR)Glutathione PeroxidaseApoptosisPINK1/ParkinATP SynthaseNa channelsNa+ channelsMitochondrial AutophagyPTEN-induced kinase 1/ParkinInhibitorinhibitorinhibit

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