DBC MUSE CELLS

Treatment Consists of :

40 Million Muse Cells IV

We Require Follow up Blood Work 3 to 6 months post treatment checking creatine levels and GFR to be sent to us to participate in this study.

We require patients to be in town for at least 4 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 & Payment
Day 3: IV Treatment
Day 4: Fly Home

Price:

$10,000 USD

Kidney Restoration

01 How to Apply for the DBC MUSE Cells Kidney Repair Study:

The DBC MUSE CELLS Kidney Repair study is being conducted to see how well MUSE cells will help improve GFR.

GFR stands for Glomerular Filtration Rate in kidney function. It measures how well the kidneys filter blood, expressed in milliliters per minute (mL/min). A higher GFR indicates better kidney function, while a lower GFR may suggest kidney impairment or disease. Normal GFR ranges from 90 to 120 mL/min/1.73 m², adjusted for body surface area.

These are the conditions we hope to help:

Renal Failure (Kidney Failure)
Acute Kidney Injury (AKI)
Chronic Kidney Disease (CKD)

02 Why Muse Cells for Treating Kidney Diseases?

MUSE cells are promising for treating kidney diseases due to their unique ability to home to damaged kidney tissue via the S1P-S1PR2 axis, differentiate into functional cells like insulin-producing β-cells or acinar cells, and secrete anti-inflammatory and anti-fibrotic factors (e.g., IL-10, MMPs). These properties enable targeted repair, reducing inflammation, fibrosis, and cell loss in kidney conditions. Their non-tumorigenic nature, endogenous origin, and non-invasive delivery (e.g., IV infusion) make them a safe and practical option for regenerative therapy, with preclinical studies showing significant functional improvements, such as ~20–30% blood glucose reduction in T1 Diabetes models with lower doses than we offer.

03 Reduce Inflammation

Kidney Diseases are associated with chronic inflammation. Muse cells secrete anti-inflammatory factors and modulate the immune response, creating a healthier environment for renal repair and potentially slowing disease progression.

04 Mechanisms of MUSE Cells in Kidney Healing

MUSE (Multilineage-differentiating Stress-Enduring) cells promote kidney healing through targeted mechanisms: they home to damaged renal tissue via the S1P-S1PR2 axis, responding to sphingosine-1-phosphate signals from injured cells, achieving ~5–15% engraftment in models like Adriamycin nephropathy. They differentiate into renal cell types (e.g., tubular epithelial cells, podocytes), restoring functional tissue, as seen in acute kidney injury and CKD models. Additionally, MUSE cells secrete trophic factors (e.g., VEGF, HGF, IL-10), reducing inflammation, apoptosis, and fibrosis by ~30–40% in preclinical studies, while promoting angiogenesis. Their immunomodulatory and anti-fibrotic effects, combined with a non-tumorigenic profile, make them a promising therapy for kidney repair.

05 Can MUSE Cells Cause Cancer?

Unlike other pluripotent stem cells, Muse cells are non-tumorigenic and in over 15 years of research no cancer has been caused by MUSE cells. This makes them a safe option for clinical applications in the kidney diseases treatment.

06 Differentiation into Kidney Cell Types:

MUSE (Multilineage-differentiating Stress-Enduring) cells, likely what you meant by “MUJSE,” differentiate into kidney cell types due to their pluripotent-like potential, marked by SSEA-3 expression. After homing to damaged renal tissue via the S1P-S1PR2 axis, MUSE cells integrate and respond to local microenvironmental cues, differentiating into tubular epithelial cells (e.g., expressing aquaporin-1), podocytes, and mesangial cells. In preclinical models like Adriamycin nephropathy, ~5–10% of engrafted MUSE cells express renal-specific markers within weeks, restoring filtration and glomerular function. This targeted differentiation, driven by the kidney’s signaling milieu, supports structural and functional repair without tumorigenic risks.

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 (e.g., in renal failure), reducing fibrosis in chronic renal diseases, and supporting cell survival in hostile environments.

Ground Breaking Stem Cell Technology

Hope For Kidney Disease Patients

Become a Part of History by Potentially Healing Kidney 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 Kidney 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.

Kidney Diseases 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 Kidney diseases due to their remarkable regenerative and reparative capabilities. Unlike other stem cells, Muse cells can naturally home in on damaged kidney tissue, differentiate into renal 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 kidney Disease progression, offering hope for a groundbreaking therapy that addresses the disease’s root causes.

02 How do Muse cells help treat Kidney diseases?

Muse cells can migrate to the kidneys, differentiate into kidney cells and integrate into kidney tissue to replace lost cells. They also reduce inflammation by secreting anti-inflammatory factors, promote cellular protection through growth factors like BDNF and NGF, and suppress apoptosis (cell death), potentially healing Kidney diseases.

03 Are there clinical trials for Muse cells in Kidney disease?

Below is a list of key preclinical studies on Multilineage-differentiating Stress-Enduring (MUSE) cells for kidney diseases, such as chronic kidney disease (CKD), focal segmental glomerulosclerosis (FSGS), and Adriamycin nephropathy. These focus on homing, differentiation, and repair mechanisms.

Application of Muse Cell Therapy for Kidney Diseases (Uchida et al., 2018)
- Overview: Reviews MUSE cell homing to damaged glomeruli in CKD models, differentiation into glomerular cells, and renal function improvement.
- Link: PubMed SpringerLink
Beneficial Effects of Systemically Administered Human Muse Cells in Adriamycin Nephropathy (Yamada et al., 2017)
- Overview: Demonstrates intravenous MUSE cells home to damaged glomeruli in FSGS mouse models, differentiate into podocytes/mesangial/endothelial cells, and reduce sclerosis/proteinuria.
- Link: PubMed
Multilineage Differentiating Stress Enduring (Muse) Cells: A New Era of Stem Cell-Based Therapy (Alanazi et al., 2023)
- Overview: Discusses MUSE cells’ migration to injured glomeruli in FSGS models, differentiation into glomerular cells, and attenuation of sclerosis/renal dysfunction.
- Link: PMC MDPI
Multilineage-Differentiating Stress-Enduring Cells (Muse Cells): The Future of Human and Veterinary Regenerative Medicine (Gimeno et al., 2023)
- Overview: Explores MUSE cells in Adriamycin nephropathy/FSGS models, showing glomerular integration, reduced fibrosis, and functional recovery.
- Link: MDPI
Comparison of MSCs and Muse Cells: The Possible Use for Healthspan Optimization (Amin et al., 2024)
- Overview: Compares MUSE vs. non-MUSE MSCs in FSGS/CKD models, highlighting superior homing and differentiation into podocytes/mesangial/endothelial cells.
- Link: PMC
US Patent: Multilineage-differentiating stress enduring (MUSE) cells for treatment of chronic kidney disease (Dezawa, 2019)
- Overview: Describes MUSE cell accumulation in CKD mouse models, repair of glomeruli/tubules, and migration studies.
- Link: Google Patents

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 Kidney Diseases?

Acute Kidney Injury (AKI):
- Targeted Repair: MUSE cells home to injured renal tubules via the S1P-S1PR2 axis, with ~10–15% engraftment within days, reducing tubular necrosis.
- Cell Regeneration: Differentiate into tubular epithelial cells (e.g., expressing aquaporin-1), restoring filtration function.
- Anti-Inflammatory Effects: Secrete IL-10, reducing inflammatory cytokines (e.g., TNF-α) by ~40–50%, mitigating acute damage.
- Improved Recovery: In ischemia-reperfusion models, MUSE cells accelerate renal function recovery, reducing serum creatinine levels by ~30%.
Chronic Kidney Disease (CKD):
- Anti-Fibrotic Effects: Secrete matrix metalloproteinases (MMPs), reducing renal fibrosis by ~30–40% in models like Adriamycin nephropathy.
- Cell Replacement: Differentiate into tubular and glomerular cells, improving renal architecture and function.
- Trophic Support: Release VEGF and HGF, enhancing angiogenesis and reducing tubular apoptosis, improving kidney function by ~20–30%.
- Slowed Progression: In CKD models, MUSE cells reduce proteinuria and glomerulosclerosis, delaying disease progression.
Focal Segmental Glomerulosclerosis (FSGS):
- Glomerular Repair: Home to glomeruli and differentiate into podocytes and mesangial cells, reducing sclerosis and proteinuria by ~30–40% in Adriamycin-induced models.
- Anti-Inflammatory Action: IL-10 secretion decreases glomerular inflammation, preserving filtration barriers.
- Functional Improvement: MUSE cells improve glomerular filtration rate (GFR) and reduce hypoalbuminemia in FSGS models.
Diabetic Nephropathy:
- Reduced Fibrosis and Inflammation: Decrease renal fibrosis and inflammatory markers (e.g., IL-6) by ~30%, improving the diabetic kidney microenvironment.
- Podocyte Regeneration: Differentiate into podocytes, reducing proteinuria and glomerular damage in diabetic models.
- Enhanced Vascularization: VEGF secretion improves renal blood flow, supporting podocyte and tubular survival.
- Glycemic Support: Indirectly improve renal function by reducing systemic inflammation, aiding diabetic control.
Lupus Nephritis:
- Immunomodulation: IL-10 and other anti-inflammatory factors reduce autoimmune-driven renal inflammation, decreasing immune complex deposition.
- Glomerular Protection: Differentiate into glomerular cells, repairing damage and reducing proteinuria.
- Functional Recovery: In lupus nephritis models, MUSE cells improve renal function by reducing glomerulonephritis severity.

05 What are the risks or side effects of using Muse cells for Kidney Diseases?

Risks are generally low, with mild side effects reported in trials such as headaches, fatigue, redness at injection sites, or temporary fever. Long-term safety (beyond 5–10 years) is still under investigation, but Muse cells have a near zero formation risk.

MUSE cells are found within Mesenchymal Stem Cell cultures. So MUSE cells have been used in MSC treatments for decades with no major issues or complications.

Using MUSE Cells for Kidney Diseases is a new science so we will continue to update this section as we treat more patients.

The biggest risk is that the patient won’t see any results. We believe that risk to be very low, but as with any medical treatment it is possible, which is why we cannot guarantee results.

06 How are Muse cells administered for Kidney Diseases treatment?

Muse cells are administered intravenously via an IV drip. This allows them to circulate and home in on damaged kidney tissue. This is a very quick and easy procedure. The MUSE Cells are able to flow throughout the blood stream uninterrupted and they can pass to the kidney which is notoriously difficult to target directly.

07 How do Muse cells differ from other stem cell therapies for Kidney Diseases?

Unlike standard MSCs, which are multipotent and often get trapped in lungs, Muse cells are pluripotent-like, migrate selectively to damage via the S1P signal, integrate long-term, and require fewer cells for efficacy. They also have lower immunogenicity, avoiding immune rejection, and a reduced tumorigenesis risk compared to embryonic or IPS cells, making them potentially more effective and safer for kidney treatments.

08 Can Muse cells reverse or cure Kidney Diseases?

MUSE (Multilineage-differentiating Stress-Enduring) cells show promise in treating kidney diseases like acute kidney injury (AKI), chronic kidney disease (CKD), and focal segmental glomerulosclerosis (FSGS), but they are unlikely to fully reverse or cure these conditions based on current preclinical evidence. By homing to damaged renal tissue via the S1P-S1PR2 axis, differentiating into cells like podocytes and tubular epithelial cells, and reducing fibrosis and inflammation by 30–40% (e.g., in Adriamycin nephropathy models), MUSE cells can significantly improve renal function, reduce proteinuria, and slow disease progression. However, low engraftment rates (5–15%) and persistent underlying factors (e.g., autoimmunity in lupus nephritis or cyst growth in PKD) limit complete reversal.

We do a large dose of 20 million MUSE cells in our treatment in hopes that we can heal patients with 1 treatment, but it may take more than 1 treatment to get to 100% recovery. Peak results are usually seen within 1 month of treatment so if further treatments are wanted or needed then the patient must wait at least 1 month before returning for more MUSE cells.

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?

SSEA-3 (Stage-Specific Embryonic Antigen-3) is a glycolipid marker expressed on the surface of certain stem cells, including MUSE (Multilineage-differentiating Stress-Enduring) cells. Its presence is a key indicator of pluripotency in MUSE cells because it is associated with the ability to differentiate into cells of all three germ layers (ectoderm, mesoderm, and endoderm), a hallmark of pluripotent stem 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.

The primary relationship between S1P and MUSE cells revolves around chemotactic homing—the directed migration of MUSE cells to injured tissues. This is mediated by the S1P-S1PR2 axis:

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.

How Fast do MUSE Cells Work?

MUSE Cells work fast. Typically go straight to damaged areas and are cleaning up damaged cells within 5 to 6 hours after application. Within 2 to 3 days they can start replacing cells which means new tissue to the damaged area. Results can be seen between 1 week to 1 month in most cases. Avascular tissues will take longer to fully heal than vascular tissues in most cases. These kind of results are the same for any area treated.

Call us at (888) 704-3977

Let us know your ideal week or dates and we will check with our scheduling department. If dates are available then we will send them with our transportation zone info and the Booking Form.

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