DBC MUSE CELLS

Treatment Consists of :

40 Million Muse Cells IV

We Require the study participant to have a brain MRI completed and sent to us before coming for treatment. Then a Follow up Blood Work 3 to 6 months post treatment and a Brain MRI scan 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

Brain Restoration

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

The DBC MUSE CELLS Brain Repair study is being conducted to see how well MUSE cells will help improve brain function. We will measure this by having all participants send us a brain MRI to apply for the study. Then all participants are required to send a follow up brain MRI and new bloodwork done 3 to 6 months post treatment. These are the conditions we hope to help:

Parkinson’s Disease
Ischemic Stroke (including Subacute Lacunar Stroke)
Hemorrhagic Stroke
Amyotrophic Lateral Sclerosis (ALS, Lou Gehrig’s Disease)
Traumatic Brain Injury (TBI)
Alzheimer’s Disease
Dementia

(Alzheimer’s and Dementia Participants will be required to complete a cognitive exam with our doctors before treatment. We will then require a follow up cognitive exam to be completed by the participants doctor back home 3 to 6 months post treatment with results sent to us for the study.)

02 How do Brain MUSE Cells work?

Ischemic Stroke (including Subacute Lacunar Stroke): MUSE cells home to the infarct area, phagocytose apoptotic cells, differentiate into neurons and oligodendrocytes, promote angiogenesis and neurogenesis, and reduce excitotoxicity, leading to sustained motor and cognitive recovery.
Hemorrhagic Stroke: MUSE cells differentiate into neural cells, modulate microglia from pro-inflammatory to reparative states, reduce hematoma expansion, and support neural circuit reconstruction for improved motor function.
Amyotrophic Lateral Sclerosis (ALS): MUSE cells protect motor neurons through neurotrophic factors like BDNF and HGF, reduce neuroinflammation, and replenish lost cells to slow disease progression and maintain motor function.
Traumatic Brain Injury (TBI): MUSE cells home to the injury site, differentiate into neural and glial cells, reduce secondary damage like oxidative stress, and enhance brain plasticity for better behavioral recovery.
Parkinson’s Disease: MUSE cells differentiate into dopaminergic neurons, provide neuroprotection via trophic factors, and modulate inflammation to slow neuron loss and improve motor symptoms.
Alzheimer’s Disease: MUSE cells promote hippocampal neurogenesis, clear amyloid plaques through phagocytosis, and reduce neuroinflammation to potentially improve cognitive function.
Multiple Sclerosis (MS): MUSE cells shift pro-inflammatory microglia to reparative states and promote remyelination by differentiating into oligodendrocytes, aiding in myelin repair and reducing demyelination effects.

03 Why Muse Cells for Treating Brain Issues & Diseases?

Multilineage-differentiating stress-enduring (MUSE) cells are a unique subset of pluripotent stem cells derived from mesenchymal tissues. Their distinct properties make them a promising therapeutic option for brain issues and diseases, including acute injuries and chronic neurodegenerative conditions. Unlike other stem cells or conventional treatments, MUSE cells offer targeted, regenerative, and safe solutions for complex brain pathologies. Below is a concise explanation of why MUSE cells stand out for treating brain issues.

MUSE cells are a promising option for brain issues due to their ability to regenerate neural tissue, reduce inflammation, protect neurons, and home to damage sites with minimal risk. Their advantages over conventional treatments and other stem cells make them a cutting-edge choice, though still experimental.

03 Reduce Inflammation

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

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

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

Pluripotent Differentiation into Neural Cells
- Why It Matters: Brain injuries and diseases often involve neuron, astrocyte, or oligodendrocyte loss, disrupting neural circuits. MUSE cells can spontaneously differentiate into these cell types, replacing damaged tissue and rebuilding functional networks.
- Advantage: Unlike standard mesenchymal stem cells (MSCs), which have limited neural differentiation, MUSE cells’ pluripotency (expressing markers like SSEA-3, Oct4) enables robust neuron/glial cell formation tailored to the brain’s needs.
- Evidence: Preclinical mouse models of ischemic stroke show MUSE cells differentiating into neurons and oligodendrocytes, with 28% engraftment and motor recovery up to 84 days (PubMed ID: 34042617). In vitro studies confirm neural marker expression.
Selective Homing to Damaged Brain Sites
- Why It Matters: Precise delivery to injury sites is critical in the brain’s complex structure. MUSE cells migrate to damaged areas via sphingosine-1-phosphate (S1P) signaling, crossing the blood-brain barrier.
- Advantage: Intravenous administration allows non-invasive, targeted repair without surgery or genetic modification, unlike other cell therapies requiring direct injection.
- Evidence: Rodent stroke models demonstrate MUSE cells accumulating in infarct zones within days, enhancing repair efficiency (PMC7478921). Nose-to-brain delivery in mice further boosts targeting (PubMed ID: 37428391).
Potent Immunomodulation and Anti-Inflammatory Effects
- Why It Matters: Neuroinflammation exacerbates brain damage in stroke, TBI, and neurodegenerative diseases. MUSE cells secrete anti-inflammatory factors and shift microglia to reparative M2 phenotypes.
- Advantage: Their immune-privileged nature avoids rejection without immunosuppression, unlike allogeneic transplants, and outperforms MSCs in reducing inflammation.
- Evidence: In mouse intracerebral hemorrhage (ICH) models, MUSE cells reduced inflammation and hematoma expansion, improving motor outcomes at 68 days. ALS trials (NCT04395321) showed lower neurofilament levels, indicating reduced inflammation.
Neuroprotection and Trophic Support
- Why It Matters: Protecting surviving neurons and supporting endogenous repair are key to mitigating brain damage. MUSE cells secrete neurotrophic factors (e.g., BDNF, VEGF, HGF) and transfer mitochondria/exosomes to enhance neural survival and plasticity.
- Advantage: Unlike drugs (e.g., tPA for stroke), which target specific pathways, MUSE cells provide broad neuroprotection, addressing multiple damage mechanisms.
- Evidence: In ALS mouse models (SOD1), MUSE cells extended survival and improved motor function via trophic support. Neonatal HIE trials (NCT04262214) showed cognitive/motor gains at 5 months via neuroprotection.
Non-Tumorigenic and Safe
- Safety is critical for brain therapies, given the risk of tumors or immune reactions. MUSE cells are non-tumorigenic and well-tolerated, even in allogeneic use.
- Advantage: Unlike embryonic or induced pluripotent stem cells, MUSE cells pose no tumor risk and require no immunosuppression, making them safer than other pluripotent therapies.
- Evidence: Phase 1/2 trials for stroke (NCT04326051) and SCI (jRCTa032200189) report no tumors or serious adverse events with ~15,000,000 cells, with effects lasting 6-52 weeks (https://pmc.ncbi.nlm.nih.gov/articles/PMC10686030/).
Versatility Across Acute and Chronic Conditions
- Brain issues range from acute (stroke, TBI) to chronic (ALS, Parkinson’s, Alzheimer’s). MUSE cells address all by repairing acute damage and slowing chronic degeneration.
- Advantage: Their ability to tackle diverse pathologies surpasses single-target drugs or less versatile stem cells.
- Evidence: Clinical trials show benefits in stroke (motor recovery, NCT04326051) and ALS (slowed progression, NCT04395321). Preclinical models suggest potential for Parkinson’s (dopaminergic neurons) and Alzheimer’s (plaque clearance, hippocampal neurogenesis).
Minimally Invasive Delivery
- Why It Matters: Brain treatments often require invasive procedures. MUSE cells can be delivered intravenously, leveraging their homing ability.
- Advantage: Reduces risks compared to surgical interventions or direct brain injections, improving patient accessibility and recovery.
- Evidence: Stroke and SCI trials use IV delivery, with MUSE cells crossing the blood-brain barrier to reach injury sites (https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-03842-w).

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 brain diseases treatment.

06 Differentiation into Brain Cell Types:

MUSE cells are pluripotent stem cells capable of differentiating into various cell types relevant to brain repair. Based on preclinical studies.

MUSE cells can differentiate into the following brain cell types:

Neurons:
- Differentiate into functional neurons, expressing markers like MAP2 and NeuN, to replace lost cells and restore neural circuits in conditions like ischemic stroke and ALS.
Astrocytes:
- Form astrocytes (GFAP-positive), supporting neural networks by regulating synaptic activity and providing metabolic support, beneficial in traumatic brain injury and Alzheimer’s disease.
Oligodendrocytes:
- Develop into oligodendrocytes (Olig2, MBP-positive), promoting remyelination of axons, critical for multiple sclerosis and stroke recovery.
Dopaminergic Neurons:
- Differentiate into dopamine-producing neurons (TH-positive), potentially restoring motor function in Parkinson’s disease 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 brain diseases, and supporting cell survival in hostile environments.

Ground Breaking Stem Cell Technology

Hope For Brain Issues & Disease Patients

Become a Part of History by Potentially Healing Brain Issues & 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 Brain Issues & 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.

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

02 How do Muse cells help treat Brain Disease?

Muse cells can migrate to the brain, differentiate into neural cells and integrate into brain 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 brain disease hallmarks like memory loss.

03 Are there clinical trials for Muse cells in Brain Issues & diseases?

There are clinical trials evaluating MUSE cells (often referred to as CL2020 ) for brain-related conditions, primarily focused on ischemic stroke, amyotrophic lateral sclerosis (ALS), and hypoxic-ischemic encephalopathy (HIE) in neonates. These are based on searches from ClinicalTrials.gov, PubMed, and related registries. No dedicated trials were found for traumatic brain injury (TBI), Parkinson’s disease, Alzheimer’s disease, or multiple sclerosis (MS), though preclinical research exists for some. Below is a list of relevant trials, including titles, phases, registry numbers, status, conditions, brief summaries, and links. Trials are early-stage (Phase 1/2), with safety and preliminary efficacy as primary focuses.

The Clinical Trial of CL2020 Cells for Neonatal Hypoxic Ischemic Encephalopathy
- Phase: Phase 1
- Registry Number: NCT04261335
- Status: Completed
- Conditions: Neonatal Hypoxic-Ischemic Encephalopathy (HIE), a brain injury from oxygen deprivation at birth leading to potential cerebral palsy or cognitive impairment.
- Summary: This trial evaluated the safety and tolerability of intravenous CL2020 in neonates with HIE undergoing hypothermia therapy. It involved dose escalation and showed no serious adverse events, with improved motor/cognitive scores at 5 months in some participants.
- Links: ClinicalTrials.gov page: https://clinicaltrials.gov/study/NCT04261335
  
  ; Publication summary: https://en.wikipedia.org/wiki/Muse_cell (section on clinical trials)
Randomized Placebo-Controlled Trial of CL2020, an Allogenic Muse Cell-Based Product, in Subacute Ischemic Stroke
- Phase: Phase 2
- Registry Number: JapicCTI-184103 (also referenced as NCT04326051 in some sources)
- Status: Completed
- Conditions: Subacute ischemic stroke, involving neuron death from blocked blood flow, leading to motor/cognitive deficits.
- Summary: This single-center, randomized, double-blind, placebo-controlled trial tested a single intravenous dose of CL2020 in 25 patients (vs. 10 placebo) 14-28 days post-stroke. It demonstrated safety (no tumors or rejection) and potential efficacy, with 40% of CL2020 patients achieving good functional outcomes (mRS ≤2 at 12 weeks) vs. 10% in placebo, sustained to 52 weeks.
- Links: Japan Clinical Trials page: https://www.clinicaltrials.jp/cti-user/trial/ShowDirect.jsp?japicId=JapicCTI-184103
  
  ; PMC publication: https://pmc.ncbi.nlm.nih.gov/articles/PMC10925866/
  
  ; Journal article: https://journals.sagepub.com/doi/10.1177/0271678X231202594
Safety and Clinical Effects of a Muse Cell-Based Product in Patients With Amyotrophic Lateral Sclerosis: Results of a Phase 2 Clinical Trial
- Phase: Phase 2
- Registry Number: jRCT2063200047
- Status: Completed
- Conditions: Amyotrophic Lateral Sclerosis (ALS), a progressive neurodegenerative disease causing motor neuron loss and muscle weakness.
- Summary: This open-label, single-center trial involved five ALS patients receiving six monthly intravenous doses of CL2020. It confirmed high tolerability with no serious treatment-related side effects. ALSFRS-R scores trended upward over 12 months, with three patients showing slowed progression; biomarkers like IL-6 and TNF-α increased temporarily, indicating immunomodulation. Links: jRCT page (via DOI reference): https://doi.org/10.1177/09636897231214370
  
  ; PMC publication: https://pmc.ncbi.nlm.nih.gov/articles/PMC10686030/
  
  summary: https://www.eurekalert.org/news-releases/1033075

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 Brain Issues & Diseases?

MUSE cells are pluripotent stem cells with unique regenerative, neuroprotective, and immunomodulatory properties, making them a promising therapy for brain issues and diseases, including acute injuries and chronic neurodegenerative conditions. Their ability to home to damaged brain tissue, differentiate into neural cell types, reduce inflammation, and promote repair offers multiple potential benefits to heal these conditions.

05 What are the risks or side effects of using Muse cells for Brain Issues & 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 brain 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 Brain Disease treatment?

Muse cells are administered intravenously via an IV drip. This allows them to circulate and home in on damaged Brain tissue. This is a very quick and easy procedure. The MUSE Cells are able to flow throughout the blood stream uninterrupted and they can cross the blood brain barrier. This makes an IV highly targeted for the brain treatment.

07 How do Muse cells differ from other stem cell therapies for Brain Issues & 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 Brain treatments.

08 Can Muse cells reverse or cure Brain Diseases?

MUSE cells are pluripotent stem cells with regenerative, neuroprotective, and immunomodulatory properties, making them a promising therapy for brain diseases such as ischemic stroke, amyotrophic lateral sclerosis (ALS), hypoxic-ischemic encephalopathy (HIE), traumatic brain injury (TBI), Parkinson’s disease (PD), Alzheimer’s disease (AD), and multiple sclerosis (MS). The question of whether MUSE cells can reverse or cure these conditions depends on the disease’s nature (acute vs. chronic), severity, and definitions of “reverse” (restore pre-disease function/structure) and “cure” (complete symptom elimination and prevention of progression).

Based on preclinical (rodent models) and early clinical trials (Phase 1/2), MUSE cells show potential to partially reverse brain disease pathology by regenerating tissue, reducing inflammation, and protecting neurons. However, a complete cure is unlikely for most conditions due to the complexity of brain damage and limited long-term human data. Below is an assessment by disease, with evidence and limitations.1. Ischemic Stroke (including Subacute Lacunar Stroke)

Potential for Reversal:
- MUSE cells can partially reverse stroke damage by regenerating neurons/oligodendrocytes, promoting angiogenesis, and reducing excitotoxicity, leading to motor and cognitive recovery.
- Evidence: Phase 2 trial (JapicCTI-184103) showed 40% of patients achieving good functional outcomes (mRS ≤2 at 12 weeks) vs. 10% in placebo, sustained to 52 weeks (https://pmc.ncbi.nlm.nih.gov/articles/PMC10925866/). Mouse middle cerebral artery occlusion (MCAO) models demonstrated 28% engraftment and functional recovery up to 84 days via neural integration (PubMed ID: 34042617).
- Impact: Significant reversal of motor/cognitive deficits in subacute stroke (14-28 days post-onset), especially in moderate cases, but full restoration to pre-stroke state is rare due to scar tissue and chronic damage.
Potential for Cure:
- A high chance for major improvement, but unlikley to cure completely,as stroke often leaves residual scarring (gliosis) and circuit loss. MUSE cells improve function but may not eliminate all deficits or prevent recurrence without addressing underlying risks.
- Limitation: Best for subacute phase; chronic stroke (>6 months) shows limited reversal due to established damage.

2. Hemorrhagic Stroke/Intracerebral Hemorrhage (ICH)

Potential for Reversal:
- MUSE cells can partially reverse ICH damage by differentiating into neural cells, reducing hematoma expansion, and modulating microglia to reparative M2 phenotypes, improving motor function.
- Evidence: Preclinical mouse ICH models showed superior motor recovery vs. non-MUSE MSCs at 68 days, with histological repair and no tumors (PubMed ID: 34042617).
- Impact: Partial restoration of function in acute/subacute ICH, but full reversal is limited by irreversible neuron loss and hematoma-induced scarring.
Potential for Cure:
- A complete cure is unlikely due to permanent tissue damage and secondary complications like edema. MUSE cells mitigate damage but cannot fully restore pre-bleed brain structure.

3. Amyotrophic Lateral Sclerosis (ALS)

Potential for Reversal:
- MUSE cells can slow ALS progression and partially reverse motor neuron loss by providing neurotrophic factors and differentiating into neural cells, improving muscle function.
- Evidence: Phase 2 trial (jRCT2063200047) showed slowed ALSFRS-R decline in 80% of patients over 10 months, with lower neurofilament levels vs. natural history (https://pmc.ncbi.nlm.nih.gov/articles/PMC10686030/). SOD1 mouse models showed extended survival and motor improvement.
- Impact: Partial reversal of motor deficits in early-stage ALS, but advanced neuron loss limits full functional restoration.
Potential for Cure:
- A cure is unlikely, as ALS is progressive and involves widespread motor neuron death. MUSE cells delay progression but cannot replace all lost neurons or halt underlying genetic drivers like SOD1 mutations.

4. Hypoxic-Ischemic Encephalopathy (HIE) in Neonates

Potential for Reversal:
- MUSE cells can significantly reverse HIE damage by suppressing microglial activation, modulating glutamate metabolism, and promoting neurogenesis, improving motor/cognitive outcomes.
- Evidence: Phase 1 trial (NCT04261335) in 9 neonates post-hypothermia showed safety and improved motor/cognitive scores at 5 months (https://clinicaltrials.gov/study/NCT04261335). Rat models confirmed functional recovery at 4 weeks via MRS/PET imaging.
- Impact: High potential for reversal in neonates due to brain plasticity, especially in mild/moderate HIE, with near-normal outcomes possible.
Potential for Cure:
- A cure is possible in mild cases, as early intervention leverages neonatal neuroplasticity. Severe HIE with extensive damage may see only partial recovery.

5. Traumatic Brain Injury (TBI)

Potential for Reversal:
- MUSE cells can partially reverse TBI damage by differentiating into neural/glial cells, reducing secondary damage (e.g., oxidative stress), and enhancing plasticity.
- Evidence: Preclinical rodent models showed improved behavioral outcomes via neurogenesis, inferred from stroke/SCI data (PubMed ID: 37428391). No dedicated TBI trials exist.
- Impact: Partial restoration of motor and cognitive functions in acute/subacute TBI, but full reversal is limited by diffuse axonal injury and scarring.
Potential for Cure:
- Unlikely to cure, as TBI often causes permanent tissue loss and complex circuit damage. MUSE cells improve function but cannot fully restore pre-injury state.

6. Parkinson’s Disease (PD)

Potential for Reversal:
- MUSE cells may partially reverse PD symptoms by differentiating into dopaminergic neurons and providing neuroprotection via trophic factors, improving motor function.
- Evidence: Preclinical mouse models of neurodegeneration show neural differentiation and circuit repair, with potential for dopaminergic neuron replacement (PubMed ID: 34042617). No clinical trials yet.
- Impact: Could reverse motor symptoms (e.g., tremors) in early PD, but full restoration of substantia nigra function is unlikely.
Potential for Cure:
- A cure is unlikely, as PD involves progressive neuron loss and non-motor symptoms (e.g., cognitive decline) that MUSE cells may not fully address.

7. Alzheimer’s Disease (AD)

Potential for Reversal:
- MUSE cells may partially reverse cognitive deficits by promoting hippocampal neurogenesis, clearing amyloid plaques via phagocytosis, and reducing neuroinflammation.
- Evidence: Mouse AD models show enhanced neurogenesis and reduced plaque burden, improving memory (PubMed ID: 37428391). No clinical trials yet.
- Impact: Potential to reverse early cognitive decline, but advanced AD with widespread atrophy is less reversible.
Potential for Cure:
- A cure is unlikely due to AD’s progressive nature and irreversible neuron loss in late stages. MUSE cells may delay progression but not eliminate pathology.

8. Multiple Sclerosis (MS)

Potential for Reversal:
- MUSE cells can partially reverse MS damage by promoting remyelination (via oligodendrocyte differentiation) and reducing autoimmune inflammation.
- Evidence: Preclinical cuprizone mouse models showed improved remyelination and anti-inflammatory effects (PubMed ID: 37428391). No clinical trials yet.
- Impact: Could reverse motor/sensory deficits in early MS by restoring myelin, but widespread lesions limit full recovery.
Potential for Cure:
- Unlikely to cure, as MS is chronic and relapsing, with complex autoimmune drivers. MUSE cells may manage symptoms but not eliminate disease.
- MUSE Cells would probably be a great first step in treating MS with a Mesenchymal stem cell treatment done a few months after to reprogram the immune system to keep the disease from coming back – Multiple Sclerosis Stem Cell Treatment

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.

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