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Chronic Pain

Chronic pain is pain that persists beyond the expected period of healing, often lasting months or years despite treatment. When the underlying cause is ischemic or neuropathic in origin, meaning the pain stems from damaged or oxygen-deprived nerves and tissue, standard pain management frequently fails to provide lasting relief.

Learn about the types of chronic pain being studied in investigational research, why conventional treatment reaches its limits, and what patients with no remaining options may want to know about ACP-01.

Chronic Pain:

What It Is and Why It Matters

Chronic pain (1)

Pain is a normal and necessary biological signal. It tells the body something is wrong and prompts action. But when pain persists long after the injury or condition that caused it has been treated, or when it develops from nerve and tissue damage that has no clear resolution, it stops being a warning signal and becomes the condition itself.

Chronic pain is broadly defined as pain lasting three months or longer. It affects more Americans than diabetes, heart disease, and cancer combined. It is the leading cause of long-term disability in the United States and one of the most undertreated conditions in modern medicine. Yet for a significant subset of patients, the pain is not just persistent. It is neuropathic, meaning it originates from damage or dysfunction in the nervous system itself, and it does not respond reliably to the medications and interventions that work for other pain types.

Neuropathic and ischemic pain conditions share a critical underlying factor: the nervous system is sending pain signals not because of ongoing injury but because the nerves themselves have been damaged, compressed, or starved of the blood supply they need to function normally. 

Standard pain management can reduce the signal. It cannot repair the underlying damage. For patients whose pain originates in compromised nerve tissue or chronically ischemic limbs, that distinction is the difference between management and resolution.

Understanding what type of chronic pain you have, where it originates, and why it has not responded to standard treatment is the foundation for finding the right path forward. 

 

Symptoms and the Lived Experience of

Chronic Pain

Chronic neuropathic and ischemic pain is notoriously difficult to describe and even more difficult for others to understand. Unlike acute pain that has a clear cause and a predictable arc, chronic pain is often invisible, unpredictable, and resistant to the treatments that help other people. Patients frequently report feeling dismissed or disbelieved before they ever receive an accurate diagnosis.

The experience varies significantly depending on the underlying condition and the nerves or tissue involved. But certain patterns appear consistently across patients living with chronic neuropathic and ischemic pain.

Pathophysiology of Advanced Ischemia

Chronic limb-threatening ischemia represents the end stage of progressive peripheral arterial obstruction, in which macrovascular and microvascular perfusion are critically impaired.

As arterial luminal narrowing progresses, distal tissue perfusion pressure falls below the threshold required to sustain cellular metabolism. Unlike intermittent claudication, where ischemia is exertional, CLTI is characterized by persistent ischemia at rest.

Sustained hypoperfusion leads to:

Reduced oxygen delivery to skeletal muscle and cutaneous tissues
Impaired removal of metabolic byproducts
Endothelial dysfunction
Capillary rarefaction
Disruption of normal inflammatory and reparative signaling

At the microvascular level, chronic ischemia alters tissue homeostasis. Capillary density may decrease, arteriolar responsiveness becomes impaired, and collateral circulation is often insufficient to compensate for proximal arterial obstruction.

As perfusion pressure declines further, tissue oxygen tension falls below viability thresholds. This physiologic shift may result in:

Ischemic rest pain due to nerve hypoxia
Failure of wound granulation
Progressive ulceration
Tissue necrosis and gangrene

The transition from compensated peripheral arterial disease to CLTI reflects a breakdown in both macrovascular inflow and microvascular adaptive capacity.

Without restoration of adequate perfusion, tissue viability becomes progressively compromised.

Common symptoms include:
 

Burning, searing, or electric shock-like pain that occurs without an obvious trigger

Persistent aching or throbbing in the affected limb or region that does not respond to standard pain relief

Allodynia, meaning pain triggered by stimuli that should not be painful, such as light touch, clothing, or a gentle breeze

Hyperalgesia, meaning an exaggerated pain response to stimuli that would normally cause only mild discomfort

Numbness, tingling, or a pins and needles sensation that is constant or recurring

Pain that is significantly worse at night, disrupting sleep and recovery

Muscle weakness or loss of coordination in the affected area

Pain that has persisted for months or years despite medications, procedures, and other interventions

A pattern of partial relief followed by return or worsening of symptoms over time

Chronic pain patient (1)

For many patients, the most exhausting aspect of chronic pain is not any single symptom but the cumulative weight of a condition that never fully lets go. Work becomes difficult or impossible. Relationships are strained. Sleep is fragmented. Activities that once brought pleasure are abandoned. The life that existed before the pain becomes harder and harder to access, and the medical system that was supposed to provide answers begins to feel like another source of frustration.

If you recognize this pattern and standard treatment has not provided lasting relief, you are not alone and you are not out of options.

Why Chronic Pain Happens

 Chronic pain rarely develops without cause. In the conditions being studied under the ACP-01 pain protocol, the underlying driver is almost always damage to nerve tissue, compromised blood supply to the nerves themselves, or both. Understanding what is causing the pain is what makes it possible to identify whether the standard treatment approach is even capable of addressing it. 

Nerve Damage from Diabetes

Diabetic polyneuropathy is one of the most common causes of chronic neuropathic pain worldwide. Chronically elevated blood sugar damages the small blood vessels that supply the peripheral nerves, a network called the vasa nervorum. When those vessels are compromised, the nerves are starved of oxygen and begin to malfunction. The result is burning, tingling, numbness, and pain in the feet and legs that progresses over time and does not resolve with pain medication alone.

Ischemia and Vascular Disease

When blood flow to the extremities is reduced by arterial disease, the nerves in the affected tissue are among the first structures to suffer. Ischemic neuropathy develops when nerves lose their blood supply and begin to deteriorate. Patients with peripheral arterial disease and chronic limb-threatening ischemia frequently experience neuropathic pain as a direct consequence of the same vascular deficit that threatens their limbs. 

Spinal Cord Injury and Damage

Trauma to the spinal cord disrupts the normal transmission of signals between the brain and the body. In many patients, this disruption does not produce silence. It produces chronic pain. Between 39 and 84 percent of people living with spinal cord injury experience chronic pain, and a significant subset describe it as one of the most debilitating consequences of their injury.  

Complex Regional Pain Syndrome

CRPS is a chronic pain condition that develops following an injury, surgery, or other triggering event, often out of proportion to what the original injury would suggest. It is characterized by severe, burning pain, changes in skin color and temperature, and sensitivity to touch that can be profoundly disabling. No disease-modifying treatment currently exists. Patients with CRPS are among the most motivated and underserved in chronic pain medicine. 

Postherpetic Neuralgia

Following a shingles outbreak, some patients develop persistent nerve pain in the area affected by the rash. This is postherpetic neuralgia, and it can last for months or years after the infection has resolved. Standard treatments including gabapentin and lidocaine patches reduce the signal for some patients but do not address the underlying nerve damage driving it. 

Phantom Limb Pain

The majority of patients who undergo amputation experience pain perceived in the limb that is no longer there. Phantom limb pain is real, neurologically grounded, and notoriously difficult to treat. For patients who have lost a limb to CLTI or vascular disease, it adds a layer of chronic pain on top of an already significant disease burden.  

 Clinical Presentation

Chronic limb-threatening ischemia is the clinical manifestation of sustained, critical limb hypoperfusion. It represents a failure of compensatory vascular mechanisms and progression beyond exertional ischemia.

CLTI is typically defined by one or more of the following:

Ischemic rest pain lasting more than two weeks
Non-healing ischemic ulcers
Tissue loss or gangrene
Objective hemodynamic evidence of arterial insufficiency

Ischemic Rest Pain

Ischemic rest pain reflects inadequate perfusion at baseline metabolic demand. It most commonly involves the forefoot or toes and is frequently described as:

Burning, aching, or pressure-like pain
Worsening when the limb is elevated
Partial relief when the limb is placed in a dependent position

The positional nature of rest pain reflects critically reduced arterial inflow and diminished perfusion pressure.

Ischemic Ulceration

Ischemic ulcers in CLTI typically:

Occur on distal pressure points such as the toes, forefoot, or heel
Demonstrate poor granulation tissue formation
Heal slowly or not at all despite appropriate wound care
May be complicated by secondary infection

Inadequate tissue oxygenation impairs cellular repair mechanisms and disrupts normal wound healing cascades.

Tissue Loss and Gangrene

Advanced CLTI may progress to:

  • Dry gangrene of distal digits

  •  

    Progressive tissue necrosis

  •  

    Localized or spreading tissue compromise

These findings indicate prolonged, severe perfusion deficit and loss of tissue viability.

Left: Gangrene of the big toe - a complication of severe PAD  -  Right: Post surgical changes. Residual PAD-related symptoms including nail dystrophy, thin, shiny skin and ischemic atrophy in other toes remain.

Across these conditions, the pattern is consistent. The nerves are damaged, compressed, or deprived of the blood supply they need to function normally. Standard pain management addresses the signal. It does not repair the underlying damage or restore the vascular environment the nerves depend on. For patients whose pain has not responded to conventional treatment, that gap is where the unmet need lives.

Types of Chronic Pain

 Chronic pain is not a single condition. It is a category that encompasses dozens of distinct diagnoses, each with its own underlying mechanism, patient population, and treatment history. The conditions listed below represent the neuropathic and ischemic pain presentations being evaluated under the ACP-01 investigational pain protocol, with a focus on those where the unmet need is greatest and the mechanism fit is strongest. 

Diabetic Polyneuropathy

Nerve damage affecting multiple peripheral nerves as a result of chronic diabetes. It is the most common cause of neuropathic pain in the United States, affecting an estimated 20 million Americans. Burning pain, numbness, and tingling in the feet and legs are the hallmark symptoms. The underlying driver is microvascular damage to the vasa nervorum, the small blood vessels that supply the peripheral nerves, making it one of the strongest mechanism fits for ACP-01's angiogenic approach. 

Complex Regional Pain Syndrome (CRPS)

A severe chronic pain condition that develops following injury, surgery, or another triggering event. CRPS produces burning pain, skin and temperature changes, and extreme sensitivity to touch that is profoundly disabling and disproportionate to the original injury. No disease-modifying therapy currently exists. An estimated 200,000 Americans are living with CRPS at any given time. Patients with CRPS are among the most motivated and underserved in all of chronic pain medicine and actively seek investigational options.

Spinal Cord Injury Pain

Between 39 and 84 percent of the approximately 300,000 Americans living with spinal cord injury experience chronic pain. For many it is among the most disabling consequences of their injury, compounding the physical and functional losses that followed the original trauma. Central neuropathic pain following spinal cord injury is poorly managed by existing pharmacological options and represents one of the largest unmet needs in the chronic pain space. 

Postherpetic Neuralgia

Persistent nerve pain that develops after a shingles outbreak and remains long after the infection has resolved. Approximately one million new shingles cases occur in the United States each year and a significant portion of those patients go on to develop postherpetic neuralgia that does not respond adequately to standard treatment. Gabapentin, pregabalin, and lidocaine patches reduce symptoms for some patients but do not address the underlying nerve damage driving the pain. 

Syringomyelia

A condition in which a fluid-filled cyst forms inside the spinal cord, progressively damaging nerve fibers and causing chronic pain in approximately 59 percent of patients. There is no satisfactory pharmacological or surgical treatment for the pain component of syringomyelia. Patients living with this condition represent a high-motivation, no-option population with an established advocacy network and limited remaining conventional pathways. 

Phantom Limb Pain

Pain perceived in an amputated limb affects the majority of patients who undergo amputation. It is neurologically real, chronic, and resistant to most available treatments. For patients who have lost a limb to peripheral arterial disease or CLTI, phantom limb pain adds a layer of chronic neuropathic pain on top of an already significant disease burden. This population overlaps directly with ACP-01's existing vascular patient base. 

Ischemic Neuropathy

Nerve damage caused by insufficient blood supply to peripheral nerves. The mechanism is identical to what drives tissue loss in CLTI, except the primary injury is to nerve tissue rather than skin and muscle. Patients with peripheral arterial disease frequently carry concurrent ischemic neuropathy, making this a natural dual-indication presentation that can be addressed in a single clinical evaluation. 

Arachnoiditis

Chronic inflammation of the arachnoid membrane surrounding the spinal cord, producing severe and often intractable pain with very limited treatment options. Many patients with arachnoiditis have been through multiple interventions including surgery, nerve blocks, and spinal cord stimulation without achieving adequate or lasting relief.  

Chemotherapy-Induced Peripheral Neuropathy

Nerve damage caused by certain chemotherapy agents that persists in cancer survivors long after treatment has ended. There is currently no FDA-approved treatment for chemotherapy-induced peripheral neuropathy. Millions of cancer survivors in the United States live with ongoing burning, numbness, and pain in their hands and feet as a direct consequence of the treatment that saved their lives.

Multiple Sclerosis-Related Pain

Neuropathic pain affects a substantial subset of people living with multiple sclerosis, driven in part by ischemic damage to neural tissue secondary to MS lesions. ACP-01's investigational approach targets this ischemic component rather than the autoimmune root cause of MS itself, and is being studied as a potential adjunctive option for patients whose pain has not responded to disease-modifying therapies. 

Chiari Malformation Type I

A structural condition in which brain tissue extends into the spinal canal, frequently producing syringomyelia and chronic pain. Patients who have undergone decompression surgery without adequate pain relief represent a motivated no-option population. The condition shares an advocacy network and patient community with syringomyelia, creating a natural cluster of patients who are actively seeking alternatives. 

Post-Surgical Neuropathic Pain

Persistent nerve pain that develops following surgery and remains beyond the expected recovery period. It is estimated that between 10 and 50 percent of surgical patients develop some degree of chronic post-surgical pain depending on the procedure type, with thoracic, cardiac, and limb surgeries carrying the highest rates. For a subset of those patients the pain becomes a chronic condition in its own right, driven by nerve injury sustained during the procedure and not resolved by the healing process alone. 

The ACP-01 pain protocol includes a broad range of neuropathic pain diagnoses because the inclusion criterion captures many conditions that share an underlying ischemic or microvascular mechanism. Not every condition included in the protocol is addressed on this page. The conditions above represent those where the mechanism fit, patient motivation, and unmet clinical need are strongest. 

How Chronic Pain Is Diagnosed

 Diagnosing chronic neuropathic and ischemic pain requires more than confirming that pain is present. It requires understanding where the pain originates, what is driving it, and why it has not responded to standard treatment. That distinction is what separates a management plan that addresses the surface from one that targets the underlying cause. 

chronic pain exam

Clinical History and Pain Assessment 

The diagnostic process begins with a detailed conversation about when the pain started, what it feels like, where it is located, what makes it better or worse, and what treatments have already been tried. Clinicians use validated pain scoring tools to quantify severity and track changes over time. A thorough history often reveals patterns that point toward a neuropathic or ischemic origin that previous evaluations may have missed or underweighted. 

Neurological Examination 

A structured physical examination assesses sensation, reflexes, muscle strength, and coordination in the affected areas. Changes in light touch, temperature perception, vibration sense, and pain response help map the distribution of nerve involvement and distinguish between central and peripheral neuropathic pain presentations. 

 Diagnostic Evaluation

Diagnosis of chronic limb-threatening ischemia requires comprehensive hemodynamic and anatomical assessment to confirm critical perfusion impairment and define revascularization options.

Evaluation typically includes:

  • Ankle-brachial index (ABI) to assess large-vessel perfusion pressure

  • Toe-brachial index (TBI) in patients with noncompressible vessels or diabetes

  • Duplex ultrasonography to evaluate arterial flow patterns and stenosis severity

  • CT angiography or MR angiography to visualize multilevel arterial disease

  • Conventional angiography for definitive anatomical mapping and procedural planning 

Hemodynamic testing helps quantify the severity of ischemia, while imaging identifies lesion location, length, and suitability for intervention.

Because CLTI is frequently associated with diffuse atherosclerosis, evaluation also includes systemic cardiovascular risk assessment. Patients with CLTI are at elevated risk for coronary and cerebrovascular events.

Accurate diagnostic staging is essential to guide revascularization strategy and limb preservation planning.

Nerve Conduction Studies and Electromyography 

Nerve conduction studies measure the speed and strength of electrical signals traveling through peripheral nerves. Electromyography assesses the electrical activity of muscles. Together they identify where along the nerve pathway damage or dysfunction is occurring and how severe it is. These tests are particularly valuable in diagnosing diabetic polyneuropathy, entrapment neuropathies, and chemotherapy-induced peripheral neuropathy. 

Quantitative Sensory Testing

A specialized assessment that measures how the nervous system responds to controlled stimuli including temperature, vibration, and pressure. Quantitative sensory testing can detect small fiber nerve damage that does not show up on standard nerve conduction studies, making it an important tool for patients whose symptoms are significant but whose conventional nerve tests appear normal.

Vascular Assessment

For patients whose pain has an ischemic component, vascular testing is an essential part of the diagnostic picture. Ankle-brachial index testing, toe pressure measurements, and duplex ultrasonography identify whether reduced blood flow to the extremities is contributing to nerve damage and pain. Patients with peripheral arterial disease or CLTI who also experience neuropathic pain symptoms should receive vascular assessment as part of their workup.

Imaging

MRI of the brain or spinal cord is used to identify structural causes of central neuropathic pain including syringomyelia, Chiari malformation, spinal cord injury changes, and MS lesions. Imaging helps confirm the anatomical source of pain and rules out conditions that require surgical or oncologic management before any other pathway is considered.

Skin Punch Biopsy

A minimally invasive procedure that samples a small piece of skin to assess the density of small nerve fibers in the tissue. Reduced intraepidermal nerve fiber density is a direct indicator of small fiber neuropathy and provides objective evidence of peripheral nerve damage in patients whose standard nerve conduction studies have returned normal results.

The Diagnostic Challenge

One of the most consistent experiences among patients with chronic neuropathic pain is the length of time it takes to receive an accurate diagnosis. Because the pain is often invisible on standard imaging and does not follow a predictable pattern, patients are frequently told their results are normal long after the underlying nerve damage is well established. A thorough diagnostic workup that includes both neurological and vascular assessment is essential for understanding what is actually driving the pain and what approaches have any realistic chance of addressing it.

How Chronic Pain Progresses Over Time

 Chronic pain rarely stays the same. Without intervention that addresses the underlying cause, neuropathic and ischemic pain conditions tend to worsen. The nerves continue to deteriorate, the vascular deficit deepens, and the pain becomes harder to manage and more disruptive to daily life. Understanding this trajectory helps patients recognize where they are in that progression and why earlier evaluation matters. 

Stage 1: Intermittent Symptoms That Are Easy to Dismiss

 Pain appears occasionally and is manageable. Tingling in the feet after a long day. Burning that comes and goes. Discomfort that seems tied to activity or position. At this stage patients frequently attribute symptoms to fatigue, aging, or a minor injury. The underlying nerve damage is already present but the body is still partially compensating. 

Stage 2: Symptoms Become Consistent and Disruptive

 Pain is now present most days. It interferes with sleep, concentration, and the ability to perform routine tasks. Patients begin modifying their behavior to accommodate the pain, avoiding activities that trigger or worsen it. Medical evaluation typically happens at this stage, often resulting in a diagnosis and a first round of pharmaceutical management. 

Stage 3: Standard Treatment Stops Working 

 Medications that provided partial relief begin to lose effectiveness or produce side effects that are difficult to tolerate. Dosages are increased. New drugs are added. Procedures are attempted. Some patients experience temporary improvement followed by return of symptoms. The treatment plan becomes increasingly complex while the underlying nerve damage continues to progress. 

Stage 4: Significant Functional Loss

 Pain is now a dominant feature of daily life. Work is difficult or no longer possible. Sleep is consistently disrupted. Relationships and social connection are strained. Patients describe withdrawing from activities and relationships they once valued. Depression and anxiety frequently develop as a consequence of sustained uncontrolled pain. The medical system has been engaged extensively and has not produced lasting relief. 

Stage 5: No Remaining Conventional Options

 The available pharmaceutical options have been exhausted or are no longer tolerable. Procedures including nerve blocks, spinal cord stimulation, or surgical intervention have been attempted without durable benefit or are not appropriate candidates for the patient's profile. A pain specialist has indicated that nothing further in the standard toolkit is available. This is the stage at which investigational evaluation becomes not just relevant but urgent. 

 Standard of Care

Management of CLTI focuses on restoring perfusion, preventing infection, and reducing systemic cardiovascular risk.

Core components of care may include:

  • Aggressive cardiovascular risk factor modification

  •  

    Optimization of glycemic control in diabetic patients

  •  

    Structured wound care and offloading strategies

  •  

    Endovascular revascularization procedures such as angioplasty or stenting

  •  

    Surgical bypass for suitable anatomical candidates

  •  

    Infection management, including antibiotic therapy when indicated

Treatment decisions are individualized and depend on:

  • Vascular anatomy and lesion distribution

  •  

    Degree of tissue loss

  •  

    Comorbid conditions such as diabetes or renal disease

  •  

    Functional status and overall surgical risk

CLTI management typically requires coordinated, multidisciplinary care involving vascular surgeons, interventional specialists, wound care teams, endocrinologists, and cardiology providers.

Timely revascularization is a key determinant of limb-related outcomes.

 Current Treatment for Chronic Pain

 Treatment for chronic neuropathic and ischemic pain focuses on reducing the pain signal, improving function, and managing the psychological impact of living with persistent pain. For most patients the approach is multimodal, combining medications, procedures, and supportive therapies. The challenge is that none of these approaches address the underlying nerve damage or vascular deficit driving the pain. They manage what the patient feels without changing what is causing it. 

 Anticonvulsants and Antidepressants 

 Gabapentin, pregabalin, and certain tricyclic and serotonin-norepinephrine reuptake inhibitor antidepressants are the most commonly prescribed medications for neuropathic pain. They work by modulating abnormal nerve signaling rather than targeting the source of damage. They are effective for some patients and inadequate for many others. 

Topical Agents 

Lidocaine patches and capsaicin preparations can reduce localized neuropathic pain without systemic side effects. They are useful adjuncts for some patients, particularly those with postherpetic neuralgia or focal neuropathic presentations. Their effect is limited to the surface area of application and does not extend to deeper nerve structures. 

Opioid Therapy 

 Opioids are sometimes prescribed for chronic neuropathic pain when other options have failed. Evidence for their long-term effectiveness in neuropathic pain specifically is limited, and the risks of dependence, tolerance, and side effects are significant. Most pain specialists now reserve opioids for carefully selected patients and as part of a broader multimodal plan rather than as a primary approach. 

 Nerve Blocks and Interventional Procedures  

 Targeted injections of local anesthetic or corticosteroid around specific nerves or nerve clusters can provide temporary relief for some neuropathic pain presentations. Sympathetic nerve blocks are used in CRPS. Epidural injections are used for spinal pain. The relief these procedures provide is frequently temporary, and repeated procedures carry cumulative risk. They do not modify the underlying nerve damage. 

 Spinal Cord Stimulation 

 An implanted device delivers low-level electrical impulses to the spinal cord to interrupt pain signaling. Spinal cord stimulation is used for CRPS, failed back surgery syndrome, and certain peripheral neuropathy presentations. It is effective for a subset of patients and provides meaningful relief when it works. It does not halt nerve deterioration and requires ongoing management of the implanted hardware.  

 Physical and Occupational Therapy  

 Structured rehabilitation addresses the functional consequences of chronic pain, helping patients maintain strength, mobility, and independence. Desensitization techniques are used in CRPS. Graded motor imagery and mirror therapy have shown benefit for phantom limb pain and CRPS in some patients. These approaches improve quality of life and function but do not resolve the underlying pain generator. 

Chronic pain has significant psychological dimensions. Cognitive behavioral therapy, acceptance and commitment therapy, and other pain psychology approaches help patients develop coping strategies, reduce catastrophizing, and improve function despite ongoing pain. They are an important component of comprehensive pain care. They do not treat the nerve damage or vascular deficit underlying the pain.
 
Some patients work through every available option with discipline and commitment and still live with pain that dominates their days. Medications that were partially effective stop working. Procedures that provided temporary relief stop holding. The treatment team has nothing new to offer. At that point the conversation about what comes next is not a conversation about giving up. It is a conversation about what else might be possible. That is where investigational research becomes relevant.

 When Patients Explore Investigational Options

For some patients with chronic neuropathic and ischemic pain, there comes a point where the medical system has done everything it can and the pain remains. Every medication class has been tried. Every appropriate procedure has been attempted. A pain specialist has indicated that nothing further is available in the standard toolkit. And the pain is still there, every day, shaping every decision and limiting every possibility.

That moment is one of the most isolating experiences in medicine. Not because the care was inadequate, but because the underlying biology has outpaced what existing treatments are designed to address. Standard pain management was built to reduce the signal. It was not built to repair the nerve damage or restore the vascular environment that is generating it. For patients whose pain originates in ischemic or structurally damaged nerve tissue, that gap is the reason treatment has not worked. It is not a personal failure. It is a gap in what currently exists.

That is exactly the patient population investigational clinical research is designed to serve.

Why Patients Begin Looking Further

Patients with chronic neuropathic and ischemic pain may explore investigational options when pain has persisted for a year or more despite appropriate multimodal treatment; multiple medication classes have been tried and have failed to provide lasting relief; interventional procedures including nerve blocks or spinal cord stimulation have not produced durable benefit; a pain specialist or neurologist has indicated that no additional conventional intervention is available; or the functional and psychological impact of the pain has reached a level that is no longer sustainable.

Seeking investigational evaluation is not a last resort born of desperation. It is an informed decision made by patients who understand their condition, have done the work that was asked of them, and are not willing to accept a future defined entirely by pain they cannot control.

What Investigational Evaluation Involves

Investigational evaluation is a structured clinical review conducted under regulated research protocols. It begins with a thorough assessment of medical history, prior diagnostic workup, current pain presentation, and treatment history to determine whether a patient meets the eligibility criteria for a research study.

Hemostemix is evaluating ACP-01, an investigational autologous cell therapy derived from a patient's own blood, in patients with chronic neuropathic and ischemic pain conditions. ACP-01 is being studied for its potential to support blood vessel growth, improve tissue perfusion, and create an environment in which damaged nerves have access to the oxygen and nutrients required for repair.

 

chronic pain pt consult (2)

Hemostemix's Investigational Approach

 ACP-01 is an investigational autologous angiogenic cell therapy derived from a patient's own blood. Because the cells come from the patient's own body, there is no risk of immune rejection and no need for donor matching. ACP-01 is being studied across multiple ischemic and neuropathic pain conditions for its potential to support vascular repair, improve nerve perfusion, and address the microvascular deficit that underlies many forms of chronic neuropathic pain.

What ACP-01 Is

ACP-01 is an investigational autologous angiogenic cell therapy derived from a patient's own blood. Because the cells come from the patient's own body, there is no risk of immune rejection and no need for donor matching. ACP-01 is being studied across multiple ischemic and neuropathic pain conditions for its potential to support vascular repair, improve nerve perfusion, and address the microvascular deficit that underlies many forms of chronic neuropathic pain.

How It Works

The process involves a standard blood draw, laboratory isolation and preparation of the angiogenic precursor cells, and reinjection into the area of ischemia using catheter-based techniques. No general anesthesia is required and most patients return to normal activities shortly after. 

What It Is and What It Isn't

ACP-01 is not an approved treatment. It is not a replacement for ongoing pain management or medical care. It does not guarantee specific outcomes. It is a structured, science-driven pathway for patients with chronic neuropathic and ischemic pain who have exhausted standard options and want to understand whether research participation may be appropriate for their clinical profile.

 If you have chronic pain that has not responded to conventional treatment and you have been told that further intervention is not possible, a clinical evaluation with Hemostemix may help determine whether investigational research is an appropriate next step for your situation. Our team reviews each case individually and is committed to honest, transparent communication about what this process involves and what it does not. 

 Request A Clinical Research Consultation 

If you or someone you love is living with an advanced ischemic condition and has been told that standard options are exhausted, their stories are not just inspiring. They are a reminder that there may still be a pathway worth exploring.

The next step is a conversation.

 Frequently Asked Questions

What is the difference between acute pain and chronic pain?

Acute pain is a normal biological response to injury or illness that resolves as the underlying cause heals. Chronic pain persists beyond the expected healing period, typically defined as three months or longer. In neuropathic and ischemic pain conditions, the pain is not a signal that healing is still occurring. It is the result of damage to the nerves or their blood supply that has not been reversed by standard treatment. 

How do I know if my pain is neuropathic?

Neuropathic pain has characteristic features that distinguish it from other pain types. Burning, electric shock-like, or shooting sensations are common. Pain triggered by stimuli that should not be painful, such as light touch or clothing against the skin, is a hallmark sign. Numbness and tingling that coexists with pain is another indicator. A neurologist or pain specialist can confirm a neuropathic diagnosis through clinical examination and appropriate testing. 

I have been managing my pain for years. Is it too late to explore investigational options?

It is not too late. The ACP-01 pain protocol is designed for patients with established chronic pain who have not found adequate relief through conventional treatment. A longer pain history does not automatically disqualify a patient from investigational evaluation. Our team reviews each case individually to determine whether the clinical profile is appropriate for research participation. 

Does ACP-01 treat the pain directly?

ACP-01 is not a pain medication and is not designed to block or suppress the pain signal. It is an investigational angiogenic cell therapy being studied for its potential to improve blood supply to ischemic and damaged nerve tissue. The hypothesis is that by improving the vascular environment surrounding compromised nerves, the underlying conditions driving the pain may be addressed rather than just managed at the surface. 

What conditions are included in the ACP-01 pain protocol?

The protocol includes a broad range of central and peripheral neuropathic pain diagnoses. The inclusion criterion is neuropathic pain with a confirmed diagnosis and a pain score of five or greater out of ten. Conditions being evaluated include diabetic polyneuropathy, complex regional pain syndrome, spinal cord injury pain, postherpetic neuralgia, phantom limb pain, ischemic neuropathy, syringomyelia, arachnoiditis, chemotherapy-induced peripheral neuropathy, multiple sclerosis-related pain, and Chiari malformation type I among others. 

Is ACP-01 approved for chronic pain?

No. ACP-01 is investigational and has not been approved by the FDA, Health Canada, or any other regulatory authority for the treatment of chronic pain or any other condition. It is being evaluated in structured clinical research programs under regulated protocols. 

What does the evaluation process involve?

Investigational evaluation begins with a clinical review of your medical history, prior diagnostic workup, current pain presentation, and treatment history. Our team uses this information to determine whether your clinical profile meets the criteria for research participation and to discuss what the process would involve if you proceed. 

Do I need a referral from my pain specialist or neurologist?

A referral is not required to begin the inquiry process. You can contact Hemostemix directly. We encourage you to keep your existing pain management team informed, as they hold important clinical history that helps our team understand your situation accurately and ensures your ongoing care is not disrupted. 

Can I continue my current pain medications during the evaluation process?

In most cases, yes. Investigational evaluation does not require patients to discontinue existing pain management. Protocol-specific requirements would be reviewed and discussed during the clinical evaluation process. Our team will provide clear information about what is and is not required at each stage.

What makes ACP-01 different from other treatments I have already tried?

Most existing chronic pain treatments work by reducing or blocking the pain signal at various points in the nervous system. ACP-01 is being studied for a different approach, targeting the vascular deficit that underlies ischemic and neuropathic pain conditions rather than the signal itself. For patients whose pain originates in compromised nerve blood supply, this represents a mechanistically distinct pathway from anything currently in standard clinical use.