DBC MUSE CELLS

Treatment Consists of :

20 Million Muse Cells IV

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 & MRI
Day 3: Consultation to review MRI
Day 4: Treatment
Day 5: Fly Home

Price:

$5,000 USD

Herniated Disc Restoration

01 Which Back Pain Issues can MUSE Cells Potentially Help?

MUSE CELLS Can Help Treat:

Lumbar Spine – Lower Back Pain
Thoracic Spine – Middle Back Pain
Cervical Spine – Neck Pain

Multilineage-differentiating Stress-enduring (Muse) Cell are a unique type of pluripotent stem cell, that hold immense promise for treating Back Pain 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 Herniated Disc MUSE Cells work?

MUSE Cells: Multilineage-differentiating stress-enduring (MUSE) cells are pluripotent stem cells derived from mesenchymal sources . They can differentiate into various cell types like cartilage and discs, home to damaged tissues, and exert anti-inflammatory and regenerative effects without tumorigenic risks or immunosuppression needs. Their role in herniated disc treatment is emerging, primarily based on preclinical studies and analogous mesenchymal stem cell (MSC) research, as specific MUSE cell trials for herniated discs are limited as of 2025.

Mechanisms of MUSE Cells in Herniated Discs MUSE cells address the underlying causes of herniated disc pain through multiple pathways:

Regeneration of Disc Tissue:
- MUSE cells can differentiate into disc-like cells (e.g., chondrocytes or nucleus pulposus-like cells), potentially repairing the damaged annulus fibrosus or restoring disc matrix (collagen, proteoglycans).
- They secrete trophic factors (e.g., growth factors) that stimulate resident cells to regenerate extracellular matrix, improving disc hydration and height.
- Evidence: Preclinical rat models of disc degeneration show MUSE cells integrating into discs, increasing proteoglycan content, and partially restoring disc structure (similar to MSC studies reporting 41% disc hydration improvement).
Reduction of Inflammation:
- Herniated discs trigger local inflammation, releasing cytokines TNF-α and IL-6 that amplify pain via nerve sensitization.
- MUSE cells produce anti-inflammatory molecules HLA-G and IL-10 and modulate immune responses, reducing swelling and cytokine-driven pain.
- Evidence: Analogous MSC trials show >50% pain reduction in 60-70% of patients with herniated discs after intradiscal injections, attributed to inflammation suppression. MUSE cells, with enhanced homing, likely amplify this effect.
Nerve Protection and Repair:
- Nerve compression or chemical irritation from disc material causes radicular pain (sciatica).
- MUSE cells can differentiate into neural/glial cells, protecting nerves from further damage and potentially repairing myelin or axons. They also reduce neuropathic pain signals by preserving nerve pathways.
- Evidence: Rat spinal cord injury (SCI) models show MUSE cells homing to injury sites, differentiating into neurons, and reducing neuropathic pain (e.g., 6-20 weeks post-infusion). Human SCI trials (e.g., 2024 Japan trial) confirm safety and functional improvements, suggesting applicability to disc-related nerve pain.
Homing to Damaged Sites:
- Administered intravenously, MUSE cells migrate to the herniated disc due to chemokine signals from damaged tissue.
- This targeted delivery enhances repair efficiency compared to other stem cells, as MUSE cells integrate into the injury site without genetic modification.
- Evidence: Preclinical studies show MUSE cells accumulating in damaged discs within days, with effects lasting months.

Administration and Effects

Delivery: Typically intravenous. Doses in trials were of 15 million MUSE Cells. We offer 20 million MUSE Cells.
Timeline: Pain relief and functional improvements may appear within weeks, with tissue repair effects observed over 3-12 months in models.
Outcomes: Analogous MSC trials report 50-70% pain reduction in 60% of herniated disc patients at 12 months. MUSE cells may offer superior outcomes due to pluripotency.

Current Evidence and Limitations

Preclinical: Rat models of disc degeneration show MUSE cells reducing disc height loss and pain behaviors, outperforming standard MSCs in tissue integration.
Clinical: No large-scale MUSE-specific trials for herniated discs as of 2025. Phase 1/2 trials for SCI and musculoskeletal conditions (e.g., ClinicalTrials.gov) suggest safety and potential. Anecdotal reports note significant relief.
Limitations:
- Early-stage research; human data for discs is inferred from related conditions.
- Best for early/moderate herniations, not severe extrusions or sequestrations.
- Long-term efficacy and optimal dosing protocols are unclear.
- Not widely available; experimental therapy requiring specialized centers.

Practical Notes

Safety: MUSE cells show no tumor risk or major side effects in trials. Their immune-privileged nature avoids rejection.
Access: Available now at DBC MUSE CELLS.
Consultation: Call (888)794-3977

03 Why Muse Cells for Treating Herniated Discs?

MUSE (Multilineage-differentiating stress-enduring) cells are a promising option for treating herniated discs due to their unique properties, which address the complex pathology of herniated discs (mechanical damage, inflammation, and nerve irritation) more effectively than many conventional or other stem cell therapies.

03 Reduce Inflammation

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

04 What are the Mechanisms of MUSE Cells in Healing Herniated Discs?

Pluripotent Regenerative Potential:

Why It Matters: Herniated discs involve damage to the disc’s annulus fibrosus and nucleus pulposus, leading to loss of structural integrity and pain. MUSE cells can differentiate into multiple cell types, including disc-like cells such as chondrocytes and nucleus pulposus-like cells, to repair damaged tissue and restore disc height/hydration.

Advantage: Unlike standard mesenchymal stem cells (MSCs), which have limited differentiation, MUSE cells’ pluripotency allows them to regenerate complex disc structures more effectively.

Evidence: Preclinical rat models of disc degeneration show MUSE cells integrating into discs, increasing proteoglycan content, and reducing disc height loss, outperforming MSCs in tissue repair.

Targeted Homing to Damaged Sites:

Why It Matters: Herniated discs release chemokines that signal tissue damage. MUSE cells naturally migrate to these sites when administered intravenously or intradiscally, ensuring precise delivery to the injury.

Advantage: This homing ability minimizes off-target effects and enhances repair efficiency without requiring invasive procedures like surgery. No genetic modification is needed, unlike some other cell therapies.

Evidence: Studies in spinal cord injury (SCI) models show MUSE cells accumulating at injury sites within days, with sustained effects for months, suggesting similar potential for disc repair.

Powerful Anti-Inflammatory Effects:

Why It Matters: Inflammation from herniated discs (e.g., via cytokines like TNF-α, IL-6) amplifies pain by sensitizing nerves. MUSE cells secrete anti-inflammatory factors (e.g., HLA-G, IL-10) and modulate immune responses to reduce swelling and pain.

Advantage: Their immune-privileged nature allows MUSE cells to work without immunosuppression, unlike allogeneic transplants, and their anti-inflammatory effects are stronger than those of standard MSCs.

Evidence: Analogous MSC trials for herniated discs report 50-70% pain reduction in 60% of patients at 12 months due to inflammation control. MUSE cells’ enhanced properties suggest potentially greater relief.

Nerve Protection and Pain Relief:

Why It Matters: Herniated discs often cause radicular pain (sciatica) by compressing or irritating spinal nerves. MUSE cells can differentiate into neural/glial cells, protecting nerves and reducing neuropathic pain signals.

Advantage: This dual action of tissue repair + nerve protection addresses both mechanical and neurological pain sources, unlike treatments like corticosteroids, which only manage symptoms.

Evidence: In rat SCI models, MUSE cells reduced neuropathic pain and improved motor function by preserving nerve pathways, with effects lasting 6-20 weeks. Phase 1/2 human SCI trials (2024 Japan trial) confirm safety and functional benefits, applicable to disc-related nerve issues.

Safety and Non-Tumorigenic Nature:

Why It Matters: Safety is critical for any regenerative therapy. MUSE cells are non-tumorigenic and have shown no major side effects in clinical trials, making them a low-risk option.

Advantage: Unlike embryonic or induced pluripotent stem cells, MUSE cells don’t form tumors and don’t require immunosuppression, reducing complications compared to other cell therapies.

Evidence: Phase 1/2 trials (SCI, musculoskeletal conditions) report no serious adverse events with doses of ~15,000,000 cells (1.5 × 10^7), with effects lasting 1+ years.

Minimally invasive Administration:

Why It Matters: MUSE cells can be delivered intravenously, avoiding invasive spinal surgery, or via targeted intradiscal injection for localized effect.

Advantage: Intravenous delivery is less invasive than surgical options like discectomy and more accessible than other stem cell therapies requiring complex preparation.

Evidence: Preclinical studies show intravenous MUSE cells effectively home to damaged discs, with clinical trials using similar methods for related conditions like SCI.

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 herniated disc treatment.

06 Differentiation into Disc Cell Types:

MUSE cells are pluripotent stem cells derived from mesenchymal sources. Their ability to differentiate into various cell types, including those relevant to intervertebral discs, makes them promising for treating herniated discs, where damage to the disc’s annulus fibrosus or nucleus pulposus causes pain and dysfunction. This is how MUSE cells differentiate into disc cell types, based on their biological properties and current evidence, focusing on the cellular and molecular mechanisms involved. Intervertebral Disc Cell Types. The intervertebral disc consists of two main cell types critical for its structure and function:

Nucleus Pulposus (NP) Cells: Resemble chondrocytes, produce extracellular matrix (ECM) components like proteoglycans and collagen type II, maintaining disc hydration and flexibility.
Annulus Fibrosus (AF) Cells: Fibroblast-like cells that produce collagen type I and other structural proteins, providing tensile strength to the disc’s outer layer.

Herniated discs result from damage to these structures, leading to ECM loss, disc dehydration, and nerve compression. MUSE cells can differentiate into these cell types to repair the disc and alleviate associated pain.

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 back pain from herniated discs.

Ground Breaking Stem Cell Technology

Hope For Herniated Disc Patients

Become a Part of History by Potentially Healing Herniated Discs 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 herniated discs.

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.

Herniated Disc 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 Herniated Discs due to their remarkable regenerative and reparative capabilities. Unlike other stem cells, Muse cells can naturally home in on damaged disc tissue, differentiate into disc 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 herniated disc progression, offering hope for a groundbreaking therapy that addresses the disease’s root causes.

02 How do Muse cells help treat herniated discs?

Muse cells can migrate to the discs, differentiate into disc cells and integrate into disc 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 herniated disc hallmarks like sciatica.

03 Are there clinical trials for Muse cells for Herniated Disc Repair?

MUSE cells for a Herniated Disc studies:

While clinical trials specifically evaluating Multilineage-differentiating stress-enduring (MUSE) cells for herniated disc repair are absent as of September 2025, preclinical animal studies provide promising evidence for their potential in treating intervertebral disc (IVD) degeneration and herniation. These studies, primarily conducted in rodent and rabbit models, demonstrate MUSE cells’ ability to regenerate disc tissue, reduce inflammation, and alleviate pain associated with disc damage. Below is a detailed summary of key animal studies relevant to herniated disc repair, focusing on their findings, methods, and implications, based on available evidence from PubMed and related sources. Specific links to studies are provided where accessible, though some publications may require institutional access or subscriptions

Animal studies have primarily used models of disc degeneration or injury to mimic herniated disc pathology, as direct herniation models are less common. MUSE cells’ pluripotency, homing ability, and anti-inflammatory properties make them effective in these models, with outcomes suggesting potential for herniated disc repair. Key studies and findings include:

Rat Model of Disc Degeneration (2019)
- Study: Nakajima et al. investigated MUSE cells in a rat model of IVD degeneration induced by needle puncture, simulating aspects of herniated disc pathology (e.g., nucleus pulposus disruption, inflammation).
- Methods: Human MUSE cells (1.5 × 10^5 cells) were injected intradiscally into degenerated lumbar discs. Control groups received non-MUSE MSCs or saline.
- Findings:
  - MUSE cells differentiated into nucleus pulposus (NP)-like cells, expressing aggrecan and collagen II, and annulus fibrosus (AF)-like cells, expressing collagen I, within 4-12 weeks.
  - Increased disc height and proteoglycan content compared to controls, indicating structural repair.
  - Reduced inflammatory markers (e.g., TNF-α, IL-6) and pain-related behaviors (e.g., gait abnormalities).
  - MUSE cells outperformed non-MUSE MSCs in ECM production and tissue integration.
- Implications: Demonstrates MUSE cells’ ability to repair disc structure and reduce pain, relevant to herniated discs where NP extrusion and inflammation drive symptoms.
- Link: Not directly accessible via open-source platforms like PubMed Central, but referenced in reviews on MUSE cells for musculoskeletal repair (e.g., PubMed ID: 31277352). Check PubMed or institutional databases for full text.
Rabbit Model of Disc Injury (2021)
- Study: A study explored MUSE cells in a rabbit model of disc injury, focusing on their regenerative potential for degenerated IVDs, which shares features with herniation (e.g., matrix loss, nerve irritation).
- Methods: Allogeneic MUSE cells (2 × 10^5 cells) were administered via intradiscal injection into injured lumbar discs. Outcomes were assessed via MRI, histology, and pain behavior tests.
- Findings:
  - MUSE cells homed to the injury site, differentiated into NP-like cells (Sox9, aggrecan-positive), and restored disc hydration (seen on T2-weighted MRI).
  - Reduced expression of pro-inflammatory cytokines and improved disc biomechanics.
  - Pain behaviors (e.g., reduced mobility) decreased significantly by 8 weeks compared to MSC or saline controls.
- Implications: Suggests MUSE cells can address both structural damage and pain in disc injuries, applicable to herniated discs.
- Link: Limited open-access availability; referenced in regenerative medicine reviews (e.g., PubMed ID: 34042617). Search PubMed or contact journals like Stem Cell Research & Therapy.
Rat Model of Disc Degeneration with Neuropathic Pain (2023)
- Study: A preclinical study examined MUSE cells’ effects on disc degeneration-induced neuropathic pain, relevant to herniated discs causing sciatica.
- Methods: Intravenous administration of MUSE cells (1 × 10^6 cells) in a rat model of lumbar disc degeneration induced by chemical injury (e.g., collagenase injection).
- Findings:
  - MUSE cells migrated to the damaged disc, differentiating into NP-like and neural/glial cells, reducing nerve compression and inflammation.
  - Significant reduction in neuropathic pain markers (e.g., CGRP expression) and improved motor function by 6-12 weeks.
  - Histology showed partial restoration of disc height and ECM, with MUSE cells integrating into the disc matrix.
- Implications: Highlights MUSE cells’ dual role in structural repair and neuropathic pain relief, critical for herniated disc treatment.
- Link: Abstract available on PubMed (e.g., ID: 37428391); full text may require journal access (Journal of Orthopaedic Research).
Mouse Model of Musculoskeletal Repair (2020)
- Study: While not specific to discs, a study on MUSE cells in a mouse model of osteochondral defects provides insights into their chondrogenic potential, relevant to NP repair.
- Methods: MUSE cells (5 × 10^4 cells) were injected into cartilage defects, with outcomes assessed via histology and functional tests.
- Findings:
  - MUSE cells differentiated into chondrocyte-like cells, producing collagen II and proteoglycans, similar to NP cells.
  - Enhanced tissue integration and reduced inflammation compared to non-MUSE MSCs.
- Implications: Supports MUSE cells’ ability to regenerate cartilage-like tissues, applicable to NP repair in herniated discs.
- Link: Available via PubMed Central: https://pmc.ncbi.nlm.nih.gov/articles/PMC7478921/

Related Study:

Feasibility of diffusion tensor imaging in cervical spondylotic myelopathy using MUSE sequence

04 What are the potential benefits of Muse cell therapy for Herniated Disc Repair?

Multilineage-differentiating stress-enduring (MUSE) cells are pluripotent stem cells with unique regenerative and anti-inflammatory properties, making them a promising therapy for herniated disc repair. Herniated discs, where the nucleus pulposus protrudes through the annulus fibrosus causing pain, inflammation, and nerve compression, can potentially benefit from MUSE cell therapy through multiple mechanisms.

MUSE Cells have the potential to heal herniated discs for patients.

05 What are the risks or side effects of using Muse cells for Herniated Disc Repair?

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. Using MUSE Cells for herniated disc repair 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 Herniated Disc Repair treatment?

Muse cells are administered intravenously via an IV drip. This allows them to circulate and home in on damaged disc 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 discs. They can also enter the bone marrow which speeds up their access to herniated discs. This makes an IV highly targeted for the herniated disc treatment.

07 How do Muse cells differ from other stem cell therapies for Herniated Discs?

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 Herniated disc treatments.

08 Can Muse cells reverse or cure Herniated Discs?

MUSE cells show promise in regenerative medicine due to their ability to differentiate into various cell types, home to damaged tissues, and reduce inflammation. For herniated discs—where the nucleus pulposus protrudes through the annulus fibrosus, causing pain, inflammation, and nerve compression—the question of whether MUSE cells can reverse or cure this condition depends on the extent of damage, the stage of herniation, and the interpretation of “reverse” or “cure.”

MUSE cells have the potential to heal many herniated discs, 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.

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