DBC MUSE CELLS
Treatment Consists of :
20 Million Muse Cells IV
- Day 1: Arrive and Rest
- Day 2: Bloodwork & Payment
- Day 3: IV Treatment
- Day 4: Fly Home
Price:
$5,000 USD
Anti-Aging
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How to Apply for the DBC MUSE Cells Anti-Aging Study
This study is being conducted to check the anti-aging potential of MUSE Cells applied via an IV.
To apply you must take a DNA Methylation test from Blueprint to assess your current age and then send us a follow up test conducted 3 to 6 months post MUSE cell Treatment.
Click here to see Brian Johnson’s Blueprint DNA Methylation Test for Age Analysis
We will only accept patients that have completed this test and sent us the results before coming for treatment. DNA tests from other providers will not be accepted.
Multi-differentiating Stress-enduring (Muse) Cell are a unique type of pluripotent stem cell, that hold immense promise for treating aging due to their remarkable regenerative and reparative capabilities. Unlike other stem cells, Muse cells can naturally home in on damaged tissue, clean up damage then turn into the tissue of that area. This study will be done to verify their anti-aging benefits.
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How do MUSE Cells work for Anti-Aging?
Aging involves hallmarks like cellular senescence, DNA damage, mitochondrial dysfunction, chronic inflammation (inflammaging), and stem cell exhaustion. MUSE cells address these directly, offering a “rejuvenation” approach by restoring youthful cellular function. The goal of our study is to measure how much we can turn the clock back with MUSE Cells and measure using a DNA Methylation test.
- Cellular Replacement and Rejuvenation: By differentiating into organ-specific cells, MUSE cells replace senescent or dysfunctional ones, improving tissue vitality. In case reports, intravenous MUSE therapy reversed biological age by 10-13 years across organ systems (e.g., brain, liver, heart), as measured by DNA methylation clocks and SystemAge scores. This reduced “aging entropy” (disorder in aging processes) and slowed aging speed.
- Anti-Inflammatory and Anti-Fibrotic Effects: MUSE cells dampen chronic low-grade inflammation by modulating cytokines (e.g., lowering IL-6, IFN-γ; boosting IL-10, TGF-β), which is key to preventing age-related diseases like arthritis or neurodegeneration.
- Systemic Longevity Support: Unlike autologous aged cells, allogeneic MUSE cells from young donors (e.g., umbilical cord) maintain efficacy independent of recipient age, potentially optimizing healthspan. They promote mitochondrial health, reduce DNA modifications, and enhance overall repair, synergizing with lifestyle interventions.
- Cellular Replacement and Rejuvenation: By differentiating into organ-specific cells, MUSE cells replace senescent or dysfunctional ones, improving tissue vitality. In case reports, intravenous MUSE therapy reversed biological age by 10-13 years across organ systems (e.g., brain, liver, heart), as measured by DNA methylation clocks and SystemAge scores. This reduced “aging entropy” (disorder in aging processes) and slowed aging speed.
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Why Muse Cells for Treating Anti-Aging?
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Reduce Inflammation
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What are the Mechanisms of MUSE Cells in Anti-Aging?
MUSE (Multilineage-differentiating Stress-Enduring) cells combat aging by targeting key hallmarks such as cellular senescence, chronic inflammation, stem cell exhaustion, mitochondrial dysfunction, and tissue fibrosis. Their pluripotent-like properties enable true cellular replacement and systemic rejuvenation, distinguishing them from typical mesenchymal stem cells (MSCs) that mainly provide paracrine support. These mechanisms operate via homing, integration, and modulation, often leveraging phagocytosis and secretion of bioactive factors.1. Homing and Targeted Migration to Aged/Damaged Tissues
- MUSE cells respond to damage-associated molecular patterns (DAMPs) and stress signals like sphingosine-1-phosphate (S1P), which is elevated in aging tissues due to cellular stress and apoptosis.
- Via S1P receptor 2 (S1PR2), they extravasate from blood vessels and home to sites of senescence or degeneration (e.g., brain, liver, heart, skin).
- This immune-tolerant homing allows systemic delivery to multiple organs, addressing multi-organ aging decline.
- In anti-aging, this ensures even distribution to restore youthful tissue architecture, countering the age-related drop in endogenous MUSE numbers.
2. Phagocytosis-Dependent Differentiation and Cellular Replacement
- A hallmark mechanism: MUSE cells engulf apoptotic or senescent cells via phagocytosis, recycling their nuclear contents.
- This triggers spontaneous differentiation into host-specific cell types from all three germ layers, replacing dysfunctional cells without genetic manipulation.
- In aging contexts, this rejuvenates tissues by eliminating senescent “zombie” cells that secrete pro-inflammatory SASP (senescence-associated secretory phenotype) factors, reducing burden and restoring function.
- Evidence from models shows integration into aged organs, improving vitality and reversing epigenetic clocks (e.g., 10-13 year biological age reduction in case studies via DNA methylation analysis).
3. Paracrine Signaling and Secretome Effects
- MUSE cells secrete a rich cocktail of factors, including:
- Anti-inflammatory cytokines (e.g., IL-10, TGF-β) to suppress inflammation by downregulating pro-inflammatory IL-6, TNF-α, and IFN-γ.
- Growth factors and exosomes promoting angiogenesis (VEGF), anti-apoptosis (e.g., BDNF, HGF), and extracellular matrix remodeling to inhibit fibrosis.
- Antioxidants and mitochondrial supporters that enhance bioenergetics, reduce oxidative stress, and clear damaged mitochondria.
- These paracrine effects create a youthful microenvironment, amplifying endogenous repair and synergizing with differentiation for holistic rejuvenation.
- Unlike aged autologous cells, young-donor MUSE cells maintain robust secretome potency, independent of recipient age.
4. Epigenetic Reprogramming and Systemic Rejuvenation
- By replacing senescent cells and modulating epigenetics, MUSE cells lower aging entropy and slow aging velocity, as measured by tools like System Age or Horvath clocks.
- Low telomerase activity ensures genomic stability, preventing tumorigenesis while supporting longevity.
- They enhance stem cell niches, countering exhaustion, and promote autophagy to clear age-related debris.
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Can MUSE Cells Cause Cancer?
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Trophic and Immunomodulatory Effects:
- Secretion of Factors: MUSE cells secrete bioactive molecules such as vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), interleukin-10 (IL-10), and matrix metalloproteinases (MMPs). These factors promote angiogenesis, reduce inflammation, inhibit apoptosis, and degrade fibrotic tissue, creating a regenerative microenvironment.
- Impact: These effects are critical for mitigating chronic inflammation, reducing fibrosis in chronic liver diseases, and supporting cell survival in hostile environments.
Ground Breaking Stem Cell Technology
Hope For Living Longer and Better
Become a Part of History by Participating in the DBC MUSE CELLS Anti-Aging Study
At DBC Muse Cells, we’re pioneering the future of regenerative medicine with Muse cell therapy, a groundbreaking treatment offering hope for age related conditions.
Our cutting-edge approach, backed by promising preclinical research and clinical trials for related conditions, positions Muse cells as a beacon of hope for those seeking innovative solutions. Muse cell therapy is an experimental treatment, and while early results are encouraging, outcomes vary and cannot be guaranteed. Each patient’s response depends on individual factors, and we’re committed to transparency about the investigational nature of this therapy. At DBC Muse Cells, our expert team will guide you through the process, ensuring you’re fully informed and supported every step of the way.
LIver Disease Muse cells
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What are Muse cells?
Multilineage-differentiating Stress-enduring (Muse) Cell are a unique type of pluripotent stem cell, that hold immense promise for treating Liver diseases due to their remarkable regenerative and reparative capabilities. Unlike other stem cells, Muse cells can naturally home in on damaged liver tissue, differentiate into liver cells, and promote repair by replacing damaged cells. Their ability to modulate inflammation and integrate seamlessly into the host tissue without forming tumors makes them a safer and more effective option for restoring cognitive function. By harnessing Muse cells, we can potentially slow or reverse liver Disease progression, offering hope for a groundbreaking therapy that addresses the disease’s root causes.
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How Will We Track Anti-Aging with MUSE Cells
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Are there clinical trials for Muse cells for anti-aging?
As of October, 2025, there are no dedicated clinical trials specifically for MUSE (Multilineage-differentiating Stress-Enduring) cells as a direct treatment for anti-aging or general age reversal. MUSE cell research remains in early clinical stages, primarily focused on regenerative applications for specific age-related diseases like stroke, myocardial infarction, spinal cord injury, amyotrophic lateral sclerosis (ALS), epidermolysis bullosa, and acute respiratory distress syndrome (ARDS). These conditions often involve age-associated degeneration, where MUSE cells demonstrate anti-inflammatory, tissue-repair, and rejuvenative effects that could indirectly support anti-aging goals, such as reducing inflammaging or restoring organ function.However, the absence of explicit anti-aging trials doesn’t preclude emerging evidence from preclinical studies, case reports, and off-label use suggesting MUSE cells’ potential for broader longevity applications. For instance:
- Preclinical models show MUSE cells counter hallmarks of aging like senescence and mitochondrial dysfunction by replacing damaged cells and modulating epigenetics.
- A 2024 case series reported biological age reversal (10-13 years via DNA methylation clocks) after intravenous MUSE infusions, but this is not a formal trial.
- Reviews emphasize MUSE cells’ suitability for healthspan extension due to their non-tumorigenic, immune-tolerant profile, with calls for future trials using aging biomarkers as endpoints.
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What are the potential benefits of Muse cell therapy for Anti-Aging?
- MUSE cells can reset aging clocks by replacing senescent cells and modulating DNA methylation patterns, reducing “aging entropy” (disorder in biological processes).
- Case reports from clinics show 10-13 year reductions in biological age across organs (brain, liver, heart) post-intravenous infusion, measured via Horvath clocks and System Age scores.
- This systemic effect slows aging velocity, enhancing overall vitality and potentially extending healthspan without genetic manipulation.
- Through homing to damaged sites and spontaneous differentiation into all three germ layers, MUSE cells replace dysfunctional or lost cells, countering age-related atrophy.
- Benefits include improved organ function: e.g., cardiac repair in myocardial infarction models (enhanced ejection fraction), neural recovery in stroke trials, and wound healing in epidermolysis bullosa.
- In anti-aging, this rejuvenates tissues like skin (reduced wrinkles, better elasticity), brain (neuroprotection against decline), and liver (detoxification efficiency), restoring youthful architecture.
- MUSE cells secrete anti-inflammatory cytokines (e.g., IL-10, TGF-β) and exosomes that suppress pro-inflammatory SASP factors (IL-6, TNF-α), dampening chronic low-grade inflammation.
- Immune tolerance allows allogeneic use from young donors without immunosuppression, optimizing efficacy in elderly recipients where autologous cells are senescent.
- Potential outcomes: Lower risk of age-related diseases like arthritis, atherosclerosis, and neurodegeneration; improved immune homeostasis.
- By inhibiting fibrosis (scar tissue buildup) via matrix remodeling factors and preventing cell death through growth factors (e.g., BDNF, HGF), MUSE cells maintain tissue pliability and function.
- Evidence from ARDS and spinal injury trials shows reduced apoptosis and fibrosis, applicable to aging-related stiffness in organs like lungs, kidneys, and heart.
- This preserves mitochondrial health, reduces oxidative stress, and promotes autophagy, clearing age-accumulated debris.
- Systemic IV delivery targets multiple organs simultaneously, synergizing with lifestyle factors for holistic rejuvenation.
- Non-tumorigenic profile ensures safety for repeated dosing, unlike iPSCs.
- Preclinical data suggest improved angiogenesis, stem cell niche support, and metabolic efficiency, potentially delaying frailty and extending disease-free years.
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What are the risks or side effects of using Muse cells for Anti-Aging?
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How are Muse cells administered for Anti-Aging?
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How do Muse cells differ from other stem cell therapies for Anti-Aging?
An Easy Way to Understand How MUSE Cells Function
The easy way that Dr. Dezawa explains to understand MUSE cells is this: Think of the MUSE cells as similar to macrophages. A macrophage will go to damaged tissue and then absorb it to clean the area up. MUSE cells do the same. They sort of eat the damaged cells then turn into them, but new and perfect. So MUSE cells go to damaged tissue, clean it up and then rebuild the tissue by turning into it.
Why can MUSE Cells be Derived from Another Person?
DBC MUSE CELLS are derived from Placenta and Umbilical Cord tissue. They are found initially with Mesenchymal Stem Cells (MSCs) in these tissues. Like MSCs they don’t express Human Leukocyte Antigen (HLA) to the immune system. This makes the immune system think they are part of the recipients body and are not attacked. This makes them safe for treatments.
Why does SSEA-3 Indicates Pluripotency in MUSE Cells?
- Experimental Validation: Studies have shown that sorting for SSEA-3-positive cells from mesenchymal tissue enriches for MUSE cells with pluripotent characteristics. For example, in vitro, SSEA-3+ cells form clusters that express markers of all three germ layers, while SSEA-3-negative MSCs do not. In vivo, SSEA-3+ MUSE cells integrate into damaged tissues (e.g., liver, lungs, heart) and differentiate into functional cell types, confirming their pluripotency.
- Comparative Studies: Other pluripotent stem cells, like ESCs and iPSCs, also express SSEA-3 (along with SSEA-4 and TRA-1-60/81), but MUSE cells are unique in being endogenous, non-tumorigenic, and stress-enduring, with SSEA-3 as the primary surface marker for their identification.
How do MUSE Cells Know Where to Go?
Muse Cells have an amazing relationship with Sphingosine 1 phosphate (S1p) that allows them to detect damaged tissue and go to help heal.
- Mechanism: Injured or apoptotic cells in damaged tissues release S1P as a “danger signal.” MUSE cells express high levels of S1PR2 (Sphingosine-1-phosphate receptor 2), a specific receptor subtype on their surface. Binding of S1P to S1PR2 activates intracellular signaling pathways (e.g., involving G-proteins, Rho GTPases, and cytoskeletal rearrangements) that guide MUSE cell migration toward the S1P gradient. This process is selective: MUSE cells accumulate rapidly at injury sites (e.g., within 1–3 days post-injury in models of stroke or myocardial infarction), enabling them to integrate into the damaged area and differentiate into functional replacement cells (e.g., cardiomyocytes, endothelial cells).
Can MUSE Cells be Mixed or Used with MSCs?
MUSE Cells cannot be applied at the same time with Mesenchymal Stem Cells (MSCs). When applied together the MUSE Cells act like MSCs. We believe that the MUSE cells are possibly consuming the MSCS and taking on their characteristics, but we are not totally sure. What we do know is that if you apply them together then you only get MSC results. So at DBC MUSE CELLS we never administer MUSE Cells and MSCs together to the same patient. If MUSE cells are applied then the patient has to wait at least 1 month before getting MSCs as to not turn the MUSE Cells into more MSC like cells.