Drug development

A new medicine class for an unsolved problem

Cacti is advancing peripheral neuroplastogens — non-psychedelic compounds that target the neural plasticity mechanisms driving chronic pain, PTSD, and traumatic brain injury, without acting on the central nervous system.

Cacti Therapeutics is a pre-clinical stage company. All pipeline information on this page is illustrative of our scientific direction. Pipeline stages, timelines, and indications are subject to change. Nothing here constitutes investment advice or a clinical claim. Please consult qualified clinicians about medical decisions.

The core insight

Chronic pain is a disease of plasticity — and so is PTSD

The standard model of pain says: tissue is damaged, nerves signal danger, pain motivates healing, and pain resolves when healing does. That model explains acute pain. It does not explain why tens of millions of people continue to hurt long after injuries heal, or why trauma survivors report pain that no structural cause can account for.

What does explain this is plasticity — the nervous system's capacity to change in response to experience. When the system that processes threat and pain undergoes maladaptive plasticity, it can become persistently sensitized, amplifying signals and generating pain with little or no peripheral input.

This is the same biological substrate at work in PTSD, TBI, and substance use disorder. These are not separate diseases that happen to co-occur with pain. They share a mechanism — and Cacti is targeting it.

Illustration of brain regions involved in pain and plasticity

Nociplastic pain originates in the nervous system's altered state — not in the tissue.

The medicine class

What is a neuroplastogen?

Neuroplastogens are compounds that promote structural and functional plasticity in the nervous system — opening windows for the brain and pain circuitry to reorganize toward health.

Mechanism

Plasticity induction

Neuroplastogens promote the growth of new synaptic connections and the reorganization of neural circuits, reversing the maladaptive sensitization that drives chronic pain and related conditions.

Differentiation

Non-psychedelic

Classic psychedelics also promote plasticity — but their hallucinogenic effects and the clinical infrastructure required limit their reach. Cacti's compounds are designed to retain the plasticity benefit while eliminating psychedelic activity.

Safety thesis

Peripheral restriction

By restricting activity to the peripheral nervous system, we aim to achieve therapeutic plasticity at the pain periphery without the central nervous system effects — hallucinogenic or otherwise — that have limited previous approaches.

Peripheral receptor targets implicated in nociplastic pain and sensitization.

Mechanism of action

Targeting the periphery to reset the system

The peripheral nervous system — the sensory neurons that innervate skin, muscle, and viscera — plays a central role in initiating and maintaining sensitization. In nociplastic pain states, peripheral sensory neurons undergo lasting changes in excitability, receptor expression, and synaptic strength that continuously feed amplified signals to the spinal cord and brain.

Cacti's neuroplastogens are designed to act on these peripheral neurons to restore normal excitability and reverse maladaptive changes, interrupting the feedforward loop that keeps pain alive. Because the compounds are restricted to the periphery, they do not cross the blood-brain barrier — avoiding the cognitive and perceptual effects of centrally-acting compounds.

Acts on peripheral sensory neurons, not the brain
Designed to restore normal neuronal excitability
Non-addictive mechanism — addresses cause, not symptoms

Chemistry

Inspired by plant medicines. Improved by design.

The structural scaffolds in our pipeline are informed by naturally occurring plant compounds with established biological activity at peripheral pain targets. Starting from these chemically validated starting points, our team at Harvard Medical School's drug-discovery screening core applies medicinal chemistry principles to tune potency, selectivity, metabolic stability, and peripheral restriction.

Our scientific strategy is to identify analogs that preserve the plasticity-promoting activity of the parent scaffold while eliminating CNS penetrance and minimizing off-target activity — producing a cleaner, safer, and more developable medicine than the natural product alone.

Structural analogs derived from plant-medicine scaffolds, optimized for peripheral restriction.

Pipeline

From discovery to development

Our current programs target nociplastic pain conditions where the unmet need is highest and the mechanistic case for neuroplastogens is strongest.

Program Indication Stage

CTX-001
Lead series · peripheral neuroplastogen

Nociplastic pain
Fibromyalgia, chronic widespread pain

Lead optimization

CTX-002
PTSD-associated pain · peripheral neuroplastogen

PTSD + chronic pain
Co-occurring trauma and pain syndromes

Hit-to-lead

CTX-003
TBI pain · peripheral neuroplastogen

TBI-associated pain
Chronic pain following traumatic brain injury

Target validation

CTX-004
SUD pain · peripheral neuroplastogen

Pain + substance use disorder
Non-addictive treatment for pain in SUD patients

Discovery

Pipeline stages are illustrative. Cacti is pre-IND. Program designations and indications subject to change as science evolves.

Why these indications

Conditions where pain, trauma, and the nervous system converge

Cacti's programs target conditions where (1) the mechanistic case for neuroplasticity-based treatment is strong, (2) existing medicines fail most patients, and (3) the populations most affected are least served — including veterans.

Primary indication

Nociplastic pain

Pain conditions — fibromyalgia, chronic widespread pain, chronic pelvic pain, IBS — where altered nervous system processing rather than ongoing tissue damage or nerve injury is the driver. The largest, most poorly-served segment of the chronic pain population and the strongest case for a plasticity-targeting medicine.

PTSD-comorbid

PTSD + chronic pain

80% of PTSD patients also live with chronic pain — yet every drug on the market treats one or the other, never both together. Cacti's mechanism is designed for exactly this intersection. A particular priority for veterans, where co-occurring PTSD and pain are epidemic.

TBI-comorbid

TBI-associated pain

Traumatic brain injury disrupts pain-modulating circuits and creates lasting changes in sensory processing. Chronic headache, musculoskeletal pain, and widespread hypersensitivity are prevalent sequelae. A second priority area for veteran populations and contact-sport athletes.

SUD-comorbid

Pain in substance use disorder

The opioid crisis emerged partly because pain and addiction share neurobiology — and opioids address both temporarily, at catastrophic long-term cost. A non-addictive, mechanism-targeted medicine that addresses the pain driving opioid use is one of the highest-value opportunities in drug development.

Succulents — resilience in difficult conditions

Resilience is not the absence of pain. It is the capacity to rebuild despite it.

Our commitment

Prioritizing those who have given the most

As a Texas company, we are acutely aware of the disproportionate burden that chronic pain, PTSD, and TBI place on veterans. The VA estimates that up to 60% of veterans with PTSD also suffer from chronic pain. Suicide risk is substantially elevated when both conditions co-occur. Existing treatments, including opioids, have made this crisis worse.

Cacti's therapeutic programs and the indications we are pursuing are shaped by this reality. We are committed to developing medicines that are both safe and effective for this population — and to doing so in partnership with the institutions, researchers, and patient advocates who know them best.

Non-addictive by design — a direct response to the opioid crisis
PTSD + pain comorbidity is a primary therapeutic focus
TBI-associated pain is a core pipeline indication

G-protein coupled receptors are key mediators of peripheral pain sensitization and plasticity.

Target biology

Receptors at the intersection of pain and plasticity

Peripheral sensory neuron biology is increasingly understood as a rich target space for pain medicines. G-protein coupled receptors (GPCRs) expressed on nociceptors — the sensory neurons that detect potentially harmful stimuli — regulate both acute pain signaling and the longer-term plasticity changes that drive chronification.

Cacti's discovery program focuses on GPCR targets implicated in the transition from acute to chronic pain and in the sensitization states associated with PTSD and TBI comorbidity, with a particular emphasis on targets where the peripheral nervous system plays a primary mechanistic role and where CNS restriction offers a meaningful safety advantage.

Why it matters

"We have been treating the symptom of a disease we haven't named yet. Nociplastic pain is that disease — and neuroplasticity is its mechanism."

The scientific thesis behind Cacti's drug development program

Scientific leadership

Grounded in decades of pain research

Cacti's science is led by researchers trained at or affiliated with the world's leading pain laboratories.

Harvard Medical School

Our CSO Nara Quintão trained under Clifford Woolf in the HMS Pain Research Center and has deep ties to Harvard's drug-discovery infrastructure.

50+ publications

Our CSO has authored more than 50 peer-reviewed papers on plant medicines, natural product analgesics, and pain mechanisms. Our scientific advisory board spans pain neuroscience, immunology, and translational drug development.

Drug development track record

Our Innovation Advisor co-founded Nocion Therapeutics and Blue Therapeutics — two biotech companies targeting peripheral pain mechanisms — and brings a decade of pain-focused drug development experience to Cacti's strategy.

Meet the team & scientific advisors

Collaborate

Working at the intersection of pain, trauma, and neuroplasticity?

We are interested in scientific partnerships, translational collaborations, and conversations with investors and institutions who share our mission.

Get in touch The trauma–pain connection