2. Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR Cytoskeleton
  3. Tie PI3K Akt Cadherin Claudin
  4. Vasculotide

Vasculotide is a blood-brain barrier (BBB)-penetrant Tie2 agonist. Vasculotide binds to a unique domain of Tie2, induces receptor clustering to drive phosphorylation, activates downstream PI3K/Akt and eNOS pathways, enhances inter-endothelial cell junctions (such as VE-cadherin and claudin-5), and inhibits inflammatory adhesion molecules, ultimately stabilizing the vascular endothelial barrier and reducing its permeability. Vasculotide alleviates pulmonary microvascular leakage and microcirculatory dysfunction caused by cardiopulmonary bypass, acts as an adjuvant radioprotective agent to reduce acute radiation dermatitis, and promotes BBB recovery after focused ultrasound (FUS). Combination of Vasculotide with antibiotics reduces lung injury.

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Custom Peptide Synthesis

Vasculotide

Vasculotide Chemical Structure

CAS No. : 1359657-45-6

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Based on 1 publication(s) in Google Scholar

Other Forms of Vasculotide:

Vasculotide Related Antibodies

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Akt Akt1 Akt2 Akt3

  • Biological Activity

  • Purity & Documentation

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Description

Vasculotide is a blood-brain barrier (BBB)-penetrant Tie2 agonist. Vasculotide binds to a unique domain of Tie2, induces receptor clustering to drive phosphorylation, activates downstream PI3K/Akt and eNOS pathways, enhances inter-endothelial cell junctions (such as VE-cadherin and claudin-5), and inhibits inflammatory adhesion molecules, ultimately stabilizing the vascular endothelial barrier and reducing its permeability. Vasculotide alleviates pulmonary microvascular leakage and microcirculatory dysfunction caused by cardiopulmonary bypass, acts as an adjuvant radioprotective agent to reduce acute radiation dermatitis, and promotes BBB recovery after focused ultrasound (FUS). Combination of Vasculotide with antibiotics reduces lung injury[1][2][3][4].

In Vitro

Vasculotide (28 ng/mL; 3 h) enhances the clonogenic survival rate of irradiated HMVEChTERT cells, with a significant SER value of 1.17[2].
Vasculotide (28 ng/mL; 3 h) preserves the angiogenic capacity of HMVEChTERTs exposed to 4 Gy irradiation, resulting in the formation of tubules comparable to those of non-irradiated cells[2].
Vasculotide (15 min) stimulates the phosphorylation of Tie2 receptors in HMVEChTERTs and activates the downstream AKT pro-survival pathway[2].

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

Vasculotide Related Antibodies
In Vivo

Vasculotide (200 ng per rat; intravenous injection; single dose) preserves microcirculatory perfusion and reduces pulmonary vascular leakage in male Wistar rats during and after cardiopulmonary bypass, without altering the endogenous angiopoietin/Tie2 system[1].
Vasculotide (10 μg/kg; intraperitoneal injection; administered 24 h and 1.5 h prior to irradiation, followed by once every other day for 28 consecutive days) reduces acute cutaneous radiation injury in mice, as evidenced by a 43% reduction in the total area of severe desquamation wounds, alleviated inflammatory responses, and improved wound healing[2].
Vasculotide (10 μg/kg; i.p.; pre-irradiation only, continuous administration, post-irradiation only; total 26 days) reduces acute cutaneous radiation injury in mice exposed to 35 Gy irradiation when administered via all tested regimens (pre-irradiation, continuous administration, post-irradiation), among which the post-irradiation regimen significantly decreases the overall skin injury score by 28%[2].
Vasculotide (250 ng; intraperitoneal injection; once every 48 hours; for 3 months) reduces the superharmonic threshold pressure for focused ultrasound (FUS)-induced blood-brain barrier (BBB) permeability by 21-29% in TgCRND8 mice and accelerates BBB repair, with an 87% BBB closure rate observed 20 hours after FUS treatment in this Alzheimer's disease model[3].
Adjuvant therapy with Vasculotide (500 ng; intravenous injection; 2 administrations) combined with Ampicillin (HY-B0522) significantly reduces pulmonary permeability, ventilator-induced lung injury (VILI)-related histological damage and edema formation in mice with mechanically ventilated Streptococcus pneumoniae pneumonia, without affecting immune responses or bacterial loads[4].

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

Animal Model: Wistar (male, 375-425 g)[1]
Dosage: 200 ng
Administration: i.v.; single dose
Result: Completely preserved microcirculatory perfusion during and after CPB, with the number of continuously perfused and non-perfused vessels remaining stable throughout the experiment.
Significantly reduced Evans blue dye extravasation in lung tissue compared with untreated CPB rats.
Did not significantly reduce leakage in kidney tissue.
Did not affect circulating concentrations of angiopoietin-1, angiopoietin-2, or soluble Tie2.
Did not affect angiopoietin-1, angiopoietin-2, or Tie2 gene/protein expression in kidney or lung tissue, or endothelial adhesion molecule expression compared with untreated CPB rats.
Animal Model: athymic nude mice (7-week-old female)[2]
Dosage: 10 μg/kg
Administration: i.p.; 24 h and 1.5 h before irradiation, then every other day; 28 days
Result: Reduced skin damage scores on day 6 and day 8, with no significant difference in overall area under the curve.
Reduced mean severe desquamation wound area overall, with peak areas reduced on day 12 and day 14.
Reduced weight loss 2 days post-irradiation, with full weight recovery by day 28.
Lowered oxygenated hemoglobin (oxyHb) levels overall, with trends toward lower levels on day 5, day 9, and day 12.
Reduced myeloperoxidase bioluminescence signal 6.4-fold lower than PBS at 72 h post-irradiation, and reduced neutrophil counts in skin sections on day 5.
Reduced serum MIP-2/CXCL2 levels on day 5 post-irradiation.
Increased CD31+ microvascular endothelial cell staining-to-area ratio on day 14 post-irradiation, with no significant difference in CD45+ leukocyte staining.
Reduced ulcerated wounds by day 28 post-irradiation (1 of 5 vs. 4 of 5 in PBS group), with histological evidence of better healing.
Animal Model: athymic nude mice (7-week-old female)[2]
Dosage: 10 μg/kg
Administration: i.p.; pre-irradiation only (24 h and 1.5 h before irradiation); continuous (24 h and 1.5 h before irradiation, then every other day); post-irradiation only (starting 2 days after irradiation, then every other day); 26 days
Result: Reduced overall skin damage scores with post-irradiation treatment, with higher body weight by day 26 and significantly reduced myeloperoxidase bioluminescence on day 23 post-irradiation.
Reduced total wound size overall with pre-irradiation, continuous, and post-irradiation treatments.
Animal Model: Mixed C57/C3H background (male and female, 3 months old at study start; transgenic TgCRND8 with double amyloid precursor protein mutations KM670/671NL, V717F; non-transgenic littermate controls)[3]
Dosage: 250 ng
Administration: i.p.; every 48 hours; 3 months
Result: Reduced the ultra-harmonic threshold pressure for FUS-induced BBB permeability by 21-29% compared to all other groups.
Did not alter initial gadolinium enhancement post-FUS in either TgCRND8 or non-transgenic mice.
Accelerated BBB closure in TgCRND8 mice: at 6, 12, and 20 hours post-FUS, 26%, 17%, and 13% of focal spots remained permeable to gadolinium, respectively, leading to 87% BBB closure by 20 hours.
Resulted in 61%, 26%, and 26% of focal spots remaining permeable to gadolinium at 6, 12, and 20 hours post-FUS in non-transgenic mice, respectively, leading to 74% BBB closure by 20 hours.
Showed a statistically significant difference in BBB closure rate between Vasculotide-treated and PBS-treated TgCRND8 mice via log-rank analysis.
Led to no detectable Evans blue dye in the brain at 24 hours post-FUS in both Vasculotide-treated TgCRND8 and non-transgenic mice, indicating complete BBB impermeability.
Animal Model: C57BL/6N (female, 8-10 weeks old, 18-20 g, intranasal inoculation with 5 × 106 CFU Streptococcus pneumoniae serotype 3 followed by 6 hours of mechanical ventilation starting 24 hours post-infection)[4]
Dosage: 500 ng (first dose); 500 ng (second dose)
Administration: i.v.; 2 doses (22 hours post-infection, 1.5 hours prior to experiment termination)
Result: Significantly reduced pulmonary hyperpermeability (measured as HSA BALF/plasma ratio) compared to ampicillin monotherapy.
Reduced the percentage of lung area affected by VILI compared to ampicillin monotherapy or untreated mice.
Reduced VILI severity scores compared to ampicillin monotherapy or untreated mice.
Diminished alveolar edema formation in VILI-affected lung areas compared to ampicillin monotherapy or untreated mice.
Reduced perivascular edema formation in pneumonia-affected lung areas compared to ampicillin monotherapy or untreated mice.
Did not alter pulmonary or systemic leukocyte counts, cytokine/chemokine production, local or systemic bacterial burden, pulmonary Tie2 mRNA expression, or pulmonary Tie2 phosphorylation.
Molecular Weight

14000 (average)

CAS No.
Appearance

Solid

Color

White to off-white

Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Sealed storage, away from moisture

Powder -80°C 2 years
-20°C 1 year

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

Solvent & Solubility
In Vitro: 

DMSO : 50 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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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: ≥ 2.5 mg/mL; Clear solution

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 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: ≥ 2.5 mg/mL; Clear solution

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 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.
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.
Please enter your animal formula composition:
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).

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

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).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation

Purity: 99.84%

SDS (252 KB)

COA (248 KB) RP-HPLC (165 KB) MS (205 KB)

Handling Instructions (2659 KB)
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Vasculotide Related Classifications

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.

Keywords:

Vasculotide1359657-45-6TiePI3KAktCadherinClaudinAngiopoietin receptorPhosphoinositide 3-kinasePKBProtein kinase BAlzheimer’s diseaseTie2 receptorventilator-induced lung injuryendothelial cellsTgCRND8 miceHMVEChTERTspneumococcal pneumoniacardiopulmonary bypassblood-brain barriermale Wistar ratsInhibitorinhibitorinhibit

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