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Pancreas MUSE Cell Treatments

Pancreas MUSE Cell Treatments DBC MUSE CELLS 2025
DBC MUSE CELLS
Treatment Consists of :

20 Million Muse Cells IV

We Require Follow up Blood Work 3 to 6 months post treatment and pancreas CT scan to be sent to us to participate in this study.
We require patients to be in town for at least 5 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 & CT
  • Day 3: Review CT Consultation & Payment
  • Day 4: IV Treatment
  • Day 5: Fly Home
Price:

$5,500 USD

old Alzheimer's Disease Muse Cells
Pancreas Restoration

01

How to Apply for the DBC MUSE Cells Pancreas Repair Study:

The DBC MUSE CELLS Pancreas Repair study is being conducted to see how well MUSE cells will help improve pancreas function. We will measure this by having a CT scan done 2 days before treatment with us and then all participants are required to send a follow up CT and new bloodwork done 3 to 6 months post treatment. These are the conditions we hope to help:

  • Pancreatitis

Multilineage-differentiating Stress-enduring (Muse) Cell are a unique type of pluripotent stem cell, that hold immense promise for treating Pancreas 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

Why Muse Cells for Treating Pancreas Diseases?​

MUSE cells are promising for treating pancreatic diseases due to their unique ability to home to damaged pancreatic 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 conditions like type 1 and type 2 diabetes, acute and chronic pancreatitis, and islet transplantation failure. 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

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

04

Mechanisms of MUSE Cells in Pancreatic Healing

Homing to Damaged Tissue via S1P-S1PR2 Axis:

  • Process: Damaged or inflamed pancreatic tissues (e.g., in diabetes or pancreatitis) release sphingosine-1-phosphate (S1P), a lipid mediator that acts as a “danger signal.” MUSE cells express high levels of S1P receptor 2 (S1PR2), enabling them to detect S1P gradients and migrate selectively to injury sites. This chemotactic homing is rapid (within 1–3 days in animal models) and ensures targeted delivery without invasive procedures.
  • Impact: Intravenous or systemic administration of MUSE cells results in their accumulation in the pancreas, where they can address localized damage. For example, in mouse models of T1DM, MUSE cells engraft in the pancreas at rates of ~5–10% within days, focusing repair efforts on islet tissue.

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 Pancreas Diseases treatment. 

06

Differentiation into Pancreatic Cell Types:

  • Pluripotency: MUSE cells, marked by SSEA-3 expression, can differentiate into cells of all three germ layers, including endodermal lineages like pancreatic β-cells (insulin-producing), acinar cells (exocrine function), and ductal cells. In vitro, MUSE cells form embryoid body-like clusters that express pancreatic markers (e.g., insulin, Pdx1, amylase), and in vivo, they integrate into damaged pancreatic tissue, adopting the phenotype of the host environment.
  • Impact: This ability allows MUSE cells to replace lost or dysfunctional cells. For instance, in T1DM models, ~5–10% of engrafted MUSE cells differentiate into insulin-producing β-like cells, contributing to glycemic control.

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 pancreatitis), reducing fibrosis in chronic pancreatitis, and supporting cell survival in hostile environments like diabetic or post-surgical pancreata.
  •  
Ground Breaking Stem Cell Technology

Hope For Pancreas Disease Patients

Become a Part of History by Potentially  Healing Pancreas 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 Pancreas 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.

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

02

How do Muse cells help treat Pancreas diseases?

Muse cells can migrate to the pancreas, differentiate into pancreatic cells, oligodendrocytes, and integrate into pancreatic 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 addressing Pancreas disease hallmarks like improper insulin response and B cell function. 

03

Are there clinical trials for Muse cells in Pancreas disease?

As of 2025, there are no specific clinical trials directly targeting Pancreas Diseases with Muse cells. However, trials for related issues have been done. In this study –

In vitro differentiation of human multilineage differentiating stress-enduring (Muse) cells into insulin producing cells 

The MUSE cells were turned into insulin producing cells. It is estimated that this can occur when MUSE cells are administered via an IV such as our treatment. 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 Pancreas Diseases?

  • Type 1 Diabetes: Restores β-cells, reduces autoimmunity, improves glycemic control.
  • Type 2 Diabetes: Enhances β-cell function, reduces inflammation and insulin resistance, supports islet survival.
  • Acute Pancreatitis: Accelerates acinar/ductal repair, reduces inflammation and necrosis.
  • Chronic Pancreatitis: Decreases fibrosis, restores exocrine/endocrine function.
  • Islet Transplantation Failure: Improves graft survival, reduces rejection, enhances vascularization.

05

What are the risks or side effects of using Muse cells for Pancreas 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 Pancreas 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 Pancreas Diseases treatment?

Muse cells are administered intravenously via an IV drip. This allows them to circulate and home in on damaged pancreas 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 pancreas which is notoriously difficult to target directly.

07

How do Muse cells differ from other stem cell therapies for Pancreas 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 pancreas treatments.

08

Can Muse cells reverse or cure Pancreas Diseases?

MUSE cells show promise in treating pancreatic diseases like type 1 and type 2 diabetes, acute and chronic pancreatitis, and islet transplantation failure, but they are unlikely to fully reverse or cure these conditions based on current evidence. Their ability to home to damaged pancreatic tissue via the S1P-S1PR2 axis, differentiate into functional cells (e.g., insulin-producing β-cells), and reduce inflammation and fibrosis can significantly improve symptoms and function—e.g., reducing blood glucose by 20–30% in T1DM mouse models or decreasing fibrosis by ~30–40% in chronic pancreatitis. However, challenges like low engraftment rates (5–15%), persistent autoimmunity (T1DM), or extensive tissue damage 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. 

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