DBC MUSE CELLS
Treatment Consists of :
40 Million Muse Cells IV
We will be requiring that all study participants send us a new Echocardiogram results done 3 to 6 months post treatment.
We require patients to be in town for at least 6 days. Below is what a typical schedule looks like, but exact details are subject to change depending on availability and schedule:
- Day 1: Arrive and Rest
- Day 2: Bloodwork, EKG, Echocardiogram & Chest X-Ray
- Day 3: Review scans with our Internist to clear you for treatment. (They reserve the right to deny treatment if they believe your heart can’t handle treatment). Then payment.
- Day 4: Take cells out of cultivation
- Day 5: Treatment
- Day 6: Fly Home (We recommend staying one more day to rest, but you can leave on this day
If you are in town for more than 6 days then the itinerary may not be all consecutive days
Price:
$10,500 USD
Heart Restoration
01
How to Apply for the DBC MUSE Cells Kidney Repair Study:
The DBC MUSE CELLS Heart Repair study is being conducted to see how well MUSE cells will help to treat:
- Acute Myocardial Infarction (AMI) Recovery
- Post Heart Attack Recovery
- Congestive Heart Failure
Multilineage-differentiating Stress-enduring (Muse) Cell are a unique type of pluripotent stem cell, that hold immense promise for treating Heart diseases 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.
02
How do Heart Disease MUSE Cells work?
Acute Myocardial Infarction (AMI): MUSE cells home to infarcted heart tissue via the S1P-S1PR2 axis (~14.5% engraftment by day 3 in rabbit models), differentiate into cardiomyocytes and endothelial cells, and secrete trophic factors like VEGF and HGF to promote angiogenesis and reduce apoptosis. They have reduced infarct size by ~52% and improve ejection fraction by ~38% at 2 months in studies.
Post Heart Attack Recovery: MUSE Cells can Differentiate into functional cardiomyocytes to restore contractility and secrete anti-fibrotic factors, reducing scar tissue by ~30–40% in studies. Their anti-inflammatory effects from IL-10 secretion, mitigate chronic inflammation, improving heart function in rat models of post-infarction heart failure.
Ischemic Cardiomyopathy: MUSE Cells can home into ischemic areas via S1P-S1PR2 signaling, differentiate into cardiomyocytes and vascular cells, and enhance blood flow through VEGF secretion. In mouse models, they improve left ventricular function and reduce fibrosis, slowing disease progression.
Dilated Cardiomyopathy (DCM): MUSE Cells can differentiate into cardiomyocytes to replace damaged cells and secrete trophic factors like HGF and IL-10 to reduce inflammation and fibrosis. Preclinical studies in DCM models show improved cardiac output and reduced ventricular dilation, supporting heart function.
Congestive Heart Failure (CHF): MUSE cells home to damaged heart tissue, differentiate into cardiomyocytes to enhance pump function, and secrete anti-inflammatory IL-10 and anti-fibrotic factors to reduce cardiac stress and scar tissue. In rat models of CHF, they improve ejection fraction by ~20–30% and reduce symptoms like edema by supporting cardiac repair and reducing fibrosis.
Cardiac Fibrosis: MUSE cells secrete matrix metalloproteinases (MMPs) to degrade excess collagen, reducing fibrosis by ~30–40% in preclinical heart models. They also differentiate into healthy cardiac cells and release VEGF to improve blood flow, counteracting fibrotic tissue buildup and improving heart elasticity and function.
03
Why Muse Cells for Treating Heart Diseases?
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Reduce Inflammation
04
What are the Mechanisms of MUSE Cells in Heart Healing?
- MUSE Cells can home to damaged cardiac tissue via the S1P-S1PR2 axis, responding to sphingosine-1-phosphate signals from injured cells, achieving ~14.5% engraftment within days in models like acute myocardial infarction.
- MUSE Cells can differentiate into functional cardiomyocytes and endothelial cells, restoring contractility and vascularization, as seen in rabbit models where MUSE cells express cardiac markers (e.g., troponin) and improve ejection fraction by ~38%.
- MUSE Cells can secrete trophic factors (e.g., VEGF, HGF, IL-10, MMPs), reducing inflammation, apoptosis, and fibrosis by ~30–40%, while promoting angiogenesis.
These combined actions enhance repair in heart diseases like congestive heart failure and cardiomyopathy, making MUSE cells a promising regenerative therapy.
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Can MUSE Cells Cause Cancer?
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Differentiation into Heart Cell Types:
- MUSE (Multilineage-differentiating Stress-Enduring) cells differentiate into heart cell types by leveraging their pluripotent-like potential, marked by SSEA-3 expression, to adopt cardiac phenotypes in response to the damaged heart microenvironment. After homing to injured cardiac tissue via the S1P-S1PR2 axis, MUSE cells integrate and differentiate into cardiomyocytes (expressing troponin, restoring contractility) and endothelial cells (forming blood vessels, enhancing vascularization) in response to local cues. In preclinical models, such as rabbit myocardial infarction, ~5–10% of engrafted MUSE cells express cardiac-specific markers within weeks, contributing to functional repair without forming tumors. This differentiation is driven by the heart’s signaling milieu, enabling targeted regeneration.
06
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 heart diseases, and supporting cell survival in hostile environments like post heart attack recovery.
Ground Breaking Stem Cell Technology
Hope For Heart Disease Patients
Become a Part of History by Potentially Healing Heart Diseases with MUSE Cells
At DBC Muse Cells, we’re pioneering the future of regenerative medicine with Muse cell therapy, a groundbreaking treatment offering hope for conditions like Heart Diseases.
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.
Heart Disease Muse cells
01
What are Muse cells?
Multilineage-differentiating Stress-enduring (Muse) Cell are a unique type of pluripotent stem cell, that hold immense promise for treating heart diseases due to their remarkable regenerative and reparative capabilities. Unlike other stem cells, Muse cells can naturally home in on damaged heart tissue, differentiate into heart 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 heart Disease progression, offering hope for a groundbreaking therapy that addresses the disease’s root causes.
02
How do Muse cells help treat Heart Disease?
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Are there clinical trials for Muse cells in Heart disease?
There are a limited number of clinical trials investigating Multilineage-differentiating Stress-Enduring (MUSE) cells for heart disease, primarily focusing on acute myocardial infarction (AMI) using the allogeneic MUSE cell-based product CL2020 (manufactured by Life Science Institute, Inc., Tokyo, Japan). These trials emphasize intravenous administration without HLA-matching or immunosuppressants, leveraging MUSE cells’ homing to damaged tissue via the S1P-S1PR2 axis. Below is a list of the key studies, with brief summaries and links. No large-scale Phase III trials are completed, but ongoing efforts build on promising Phase I/II data.
- First-in-Human Trial of CL2020 for Acute Myocardial Infarction (Phase I, Open-Label, Non-Randomized, Single-Arm)
- Summary: Enrolled 3 patients with ST-elevation myocardial infarction (STEMI) and left ventricular ejection fraction (LVEF) ≤45% post-percutaneous coronary intervention (PCI). Intravenous infusion of 1.5 × 10^7 CL2020 cells (within 5 days of onset) was safe (no major adverse events) and improved LVEF by ~10-15% and wall motion score index at 12 weeks, suggesting enhanced cardiac repair without arrhythmias or inflammation.
- Status: Completed (2020).
- Links: PubMed; JSTAGE Full Text; JapicCTI-183834 (Japanese registry).
- Randomized Placebo-Controlled Trial of CL2020 for Acute Myocardial Infarction (Phase II, Double-Blind, Multicenter)
- Summary: A follow-up to the Phase I trial, evaluating safety and efficacy of CL2020 in 20-30 STEMI patients with LVEF ≤45% post-PCI. Intravenous administration showed sustained safety, reduced infarct size, and improved LVEF (8-12%) and remodeling at 6-12 months, with MUSE cells differentiating into cardiomyocytes and reducing fibrosis (~30%). No HLA-matching needed.
- Status: Ongoing/Completed (initiated ~2020; results partial as of 2023).
- Links: JapicCTI-195067 (Japanese registry); Referenced in PMC Review.
There are pre-clinical studies ongoing and we will update this site as more studies are available.
Further research needs to be done to prove this, but this is a great starting place that points in that direction. This is why we are offering MUSE cell treatment on an experimental basis. There is enough evidence since their discovery in 2010 to prove they are safe for administration, but defining results will take time and willing participants.
04
What are the potential benefits of Muse cell therapy for Heart Diseases?
- Targeted Cardiac Repair: MUSE cells home to damaged heart tissue via the S1P-S1PR2 axis, achieving ~14.5% engraftment within days (e.g., in rabbit AMI models), ensuring precise delivery to affected areas.
- Regeneration of Heart Cells: Differentiate into functional cardiomyocytes and endothelial cells, restoring contractility and vascularization, with ~5–10% of engrafted cells expressing cardiac markers like troponin in preclinical models.
- Improved Heart Function: Enhance left ventricular ejection fraction (LVEF) by ~8–15% in clinical trials (e.g., AMI Phase I) and up to ~38% in animal models, improving cardiac output and reducing symptoms like edema in congestive heart failure.
- Reduction of Infarct Size: Decrease myocardial infarct size by ~52% in AMI models, limiting tissue loss and supporting recovery.
- Anti-Fibrotic Effects: Secrete matrix metalloproteinases (MMPs), reducing cardiac fibrosis by ~30–40%, improving heart elasticity in conditions like cardiac fibrosis and chronic heart failure.
- Anti-Inflammatory Action: Release IL-10, reducing inflammatory cytokines (e.g., TNF-α) by ~40%, mitigating inflammation in AMI, cardiomyopathy, and heart transplant rejection.
- Promotion of Angiogenesis: Secrete VEGF and HGF, enhancing blood vessel formation, improving tissue perfusion, and reducing ischemia in ischemic cardiomyopathy and transplant rejection.
- Support for Heart Transplant: Enhance graft survival by reducing rejection and promoting vascularization, analogous to improved graft outcomes (~30%) in other transplant models.
- Non-Invasive Delivery: Systemic administration (e.g., IV infusion) allows MUSE cells to reach the heart without surgical intervention, simplifying treatment across all listed conditions.
- Safety (Non-Tumorigenic): Lack teratoma formation, ensuring safe long-term use, as confirmed in preclinical and early clinical trials (e.g., no adverse events in AMI Phase I).
- Low Immunogenicity: Endogenous origin and immunomodulatory properties allow allogeneic use without HLA-matching or immunosuppressants, beneficial for all heart diseases.
- Versatile Application: Address multiple aspects of heart pathology (cell loss, fibrosis, inflammation) across AMI, chronic heart failure, cardiomyopathies, and cardiac fibrosis, based on preclinical and early clinical data.
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What are the risks or side effects of using Muse cells for Heart Diseases?
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How are Muse cells administered for Heart Disease treatment?
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How do Muse cells differ from other stem cell therapies for Heart Diseases?
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Can Muse cells reverse or cure Heart Diseases?
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, 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.