DBC MUSE CELLS

Treatment Consists of :

40 Million Muse Cells IV

We Require Follow up Blood Work and a new liver ultrasound done 3 to 6 months post treatment 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, Liver ultrasound & Payment
Day 3: IV Treatment
Day 4: Fly Home

Price:

$10,000 USD

Liver Restoration

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

The DBC MUSE CELLS Liver Repair study is being conducted to see how well MUSE cells will help improve Liver function. These are the conditions we hope to help:

Liver Fibrosis/Cirrhosis Pulmonary Disease (COPD)
Alcoholic Liver Disease
Non-Alcoholic Fatty Liver Disease (NAFLD)/Non-Alcoholic Steatohepatitis (NASH)
Alcoholic Liver Disease

02 How do Liver Disease MUSE Cells work?

Liver Fibrosis/Cirrhosis: MUSE cells home to fibrotic liver tissue via the S1P-S1PR2 axis, differentiate into hepatocytes and cholangiocytes, and secrete anti-fibrotic factors (e.g., MMPs) to reduce collagen deposition by ~30–40%, improving liver architecture and function in CCl4-induced mouse models.
Acute Liver Injury (ALI): MUSE cells migrate to inflamed liver sites, differentiate into hepatic progenitor cells, and release anti-inflammatory cytokines to decrease inflammation and apoptosis by ~40–50%, accelerating recovery and enhancing survival in preclinical ALI models compared to non-MUSE MSCs.
Non-Alcoholic Fatty Liver Disease (NAFLD)/Non-Alcoholic Steatohepatitis (NASH): MUSE cells integrate into damaged hepatocytes, promote lipid metabolism through differentiation and trophic factors like HGF and VEGF, reducing steatosis and inflammation in high-fat diet mouse models, supporting metabolic restoration.
Partial Hepatectomy (Liver Resection Injury): MUSE cells home to the regenerating liver, differentiate into hepatocytes (up to 74%), cholangiocytes, sinusoidal endothelial cells, and Kupffer cells, enhancing proliferation and functional recovery in SCID mouse and pig hepatectomy models without tumorigenicity.
Viral Hepatitis-Induced Liver Damage: MUSE cells target virus-damaged areas, differentiate into functional liver cells, and modulate immune responses via IL-10 secretion to reduce chronic inflammation and fibrosis, as suggested by their efficacy in inflammatory liver injury models.
Alcoholic Liver Disease: MUSE cells repair alcohol-induced damage by homing to injured zones, differentiating into hepatocytes, and secreting protective factors to mitigate oxidative stress and steatosis, based on broader preclinical data for toxic liver injuries like CCl4 models.

03 Why Muse Cells for Treating Liver Diseases?

MUSE (Multilineage-differentiating Stress-Enduring) cells are a promising therapy for liver diseases due to their unique ability to home to damaged liver tissue via the S1P-S1PR2 axis, achieving ~5–15% engraftment in models like CCl4-induced fibrosis. They differentiate into functional hepatocytes, cholangiocytes, and other liver cells, restoring tissue integrity, while secreting trophic factors that reduce inflammation by ~40–50% and fibrosis by ~30–40%, as seen in preclinical studies of liver fibrosis and acute liver injury. Their non-tumorigenic nature, low immunogenicity, and systemic delivery enable safe, non-invasive treatment for conditions like cirrhosis, NAFLD, and post-hepatectomy recovery. Early clinical trials for other indications support translational potential, making MUSE cells a versatile regenerative option for liver repair.

03 Reduce Inflammation

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

04 What are the Mechanisms of MUSE Cells in Liver Healing?

MUSE (Multilineage-differentiating Stress-Enduring) cells promote liver healing through three key mechanisms, leveraging their pluripotent-like and stress-enduring properties:

Homing to Damaged Liver Tissue: MUSE cells migrate to injured liver sites via the S1P-S1PR2 axis, responding to sphingosine-1-phosphate (S1P) signals from damaged hepatocytes or cholangiocytes. In preclinical models, ~5–15% of infused MUSE cells engraft in the liver within days, ensuring targeted repair for conditions like cirrhosis or acute liver injury.
Differentiation into Liver Cell Types: MUSE cells, marked by SSEA-3 expression, differentiate into functional hepatocytes, cholangiocytes (bile duct cells), sinusoidal endothelial cells, and Kupffer cells in response to the liver’s microenvironmental cues. In hepatectomy models, up to 74% of engrafted MUSE cells express hepatic markers (e.g., albumin, cytokeratin-19), restoring liver function.
Trophic and Anti-Fibrotic Effects: MUSE cells secrete trophic factors (e.g., HGF, VEGF, IL-10) to reduce inflammation by ~40–50% and matrix metalloproteinases (MMPs) to decrease fibrosis by ~30–40%, as seen in NAFLD and cirrhosis models. These factors also promote angiogenesis, reduce apoptosis, and enhance tissue regeneration, creating a supportive microenvironment for liver repair.

These mechanisms collectively restore liver structure, improve function, and mitigate pathological inflammation and fibrosis in diseases like NAFLD, cirrhosis, and viral hepatitis

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 liver diseases treatment.

06 Differentiation into Liver Cell Types:

MUSE (Multilineage-differentiating Stress-Enduring) cells differentiate into liver cell types by leveraging their pluripotent-like potential, marked by SSEA-3 expression, to respond to the damaged liver microenvironment. After homing to injured liver tissue via the S1P-S1PR2 axis, driven by sphingosine-1-phosphate signals, MUSE cells integrate and adopt specific hepatic phenotypes based on local cues (e.g., growth factors like HGF or TGF-β). In preclinical models (e.g., CCl4-induced fibrosis or partial hepatectomy), ~5–15% of engrafted MUSE cells differentiate within weeks into:

Hepatocytes: Express albumin and CYP450, performing metabolic and detoxification functions, with up to 74% of engrafted cells becoming hepatocytes in hepatectomy models.
Cholangiocytes: Form bile ducts, expressing cytokeratin-19, aiding bile transport in fibrosis or viral hepatitis models.
Sinusoidal Endothelial Cells: Support vascularization, expressing CD31, enhancing liver blood flow.
Kupffer Cells: Contribute to immune regulation, expressing macrophage markers, reducing inflammation in NAFLD or acute liver injury.

This spontaneous differentiation, driven by the liver’s regenerative signals, restores functional tissue without tumorigenic risks, as confirmed in SCID mouse and pig models.

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 liver diseases, and supporting cell survival in hostile environments.

Ground Breaking Stem Cell Technology

Hope For Liver Disease Patients

Become a Part of History by Potentially Healing Liver 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 Liver 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.

LIver 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 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.

02 How do Muse cells help treat Liver Disease?

Muse cells can migrate to the liver, differentiate into hepatic cells and integrate into liver tissue to replace lost cells. They also reduce inflammation by secreting anti-inflammatory factors, promote cellular through growth factors like BDNF and NGF, and suppress apoptosis (cell death), potentially addressing liver disease hallmarks like cirrhosis.

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

MUSE cells for a liver disease studies:

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 Liver Diseases?

The potential benefits of MUSE (Multilineage-differentiating Stress-Enduring) cell therapy for liver diseases, tailored to specific conditions such as liver fibrosis/cirrhosis, acute liver injury (ALI), non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH), viral hepatitis-induced liver damage, and alcoholic liver disease. These benefits are based on preclinical evidence:

Targeted Liver Repair:
- MUSE cells home to damaged liver tissue via the S1P-S1PR2 axis, achieving ~5–15% engraftment within days (e.g., in CCl4-induced fibrosis models), ensuring precise repair in cirrhosis, ALI, NAFLD/NASH, viral hepatitis, and alcoholic liver disease.
Regeneration of Liver Cells:
- Differentiate into hepatocytes (up to 74% in hepatectomy models), cholangiocytes, sinusoidal endothelial cells, and Kupffer cells, restoring metabolic and bile transport functions, as seen in ALI and cirrhosis models expressing albumin and cytokeratin-19.
Improved Liver Function:
- Enhance detoxification and protein synthesis like albumin production by regenerating hepatocytes, improving liver enzyme profiles in NAFLD/NASH and alcoholic liver disease models.
Reduction of Inflammation:
- Secrete IL-10, reducing pro-inflammatory cytokines like TNF-α and IL-6 by ~40–50% in ALI and viral hepatitis models, alleviating inflammation in NAFLD/NASH and alcoholic liver disease.
Anti-Fibrotic Effects:
- Release matrix metalloproteinases , decreasing fibrosis by ~30–40% in cirrhosis and NAFLD/NASH models, improving liver elasticity and slowing disease progression.
Promotion of Angiogenesis:
- Secrete VEGF and HGF, enhancing vascularization and reducing ischemia in sinusoidal structures, supporting tissue survival in ALI, hepatectomy, and alcoholic liver disease.
Support for Liver Regeneration Post-Hepatectomy:
- Accelerate liver regrowth by differentiating into multiple liver cell types and promoting proliferation, as shown in SCID mouse and pig hepatectomy models, improving recovery after surgical resection.
Non-Invasive Delivery:
- Systemic administration IV infusion allows MUSE cells to reach the liver without invasive procedures, simplifying treatment for all listed conditions.
Safety (Non-Tumorigenic):
- Lack teratoma formation, ensuring safe use, as confirmed in preclinical models (e.g., up to 6 months), applicable to all liver diseases.
Low Immunogenicity:
- Endogenous origin and immunomodulatory properties allow allogeneic use without HLA-matching, reducing rejection risks across conditions, as supported by preclinical xenogeneic models.

05 What are the risks or side effects of using Muse cells for Liver 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 liver 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 Liver Disease treatment?

Muse cells are administered intravenously via an IV drip. This allows them to circulate and home in on damaged Liver 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 liver. This makes an IV highly targeted for the liver treatment.

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

Unlike standard MSCs, which are multipotent and often get trapped in the 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 Liver treatments.

08 Can Muse cells reverse or cure Liver Diseases?

MUSE cells show significant potential for treating liver diseases such as cirrhosis, acute liver injury, NAFLD/NASH, viral hepatitis, and alcoholic liver disease, but we don’t know yet if they will fully reverse or cure these conditions based on current preclinical evidence. In models like CCl4-induced fibrosis and partial hepatectomy, MUSE cells home to damaged liver tissue via the S1P-S1PR2 axis, differentiate into hepatocytes and other liver cells (~5–15% engraftment, up to 74% hepatocytes in hepatectomy), reduce fibrosis by ~30–40%, and decrease inflammation by ~40–50%, improving liver function.

MUSE cells have the potential to heal many liver diseases, but we are always careful to use the term, cure.

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, 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.

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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