A widely-used class of cholesterol-lowering drugs produces a metabolic byproduct with documented antiviral activity against rhinovirus — yet no study has connected the two for cold treatment. The mechanism is well-characterised in cholesterol biology; its application here has never been tested.
Full mechanistic analysis available under commercial agreement.
Request AccessA self-amplifying inflammatory cycle links gut-derived signals to misfolded protein accumulation in the brain, each reinforcing the other. Combining an anti-inflammatory approved for another indication with a drug that enhances a specific sleep-dependent clearance process could interrupt the cycle at two independent points — a combination never tested.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific form of iron-dependent cell death damages the receptor responsible for clearing amyloid from the brain, creating a self-reinforcing cycle of accumulation. Combining an approved iron-chelating drug with a receptor-targeted approach addresses both sides of this cycle — the first demonstration of this connection.
Full mechanistic analysis available under commercial agreement.
Request AccessPairing a cholesterol-pathway antiviral approach with an intranasal bacterial lysate that primes local immunity, stratified by individual microbiome risk profiles, targets both viral replication and host defence simultaneously — a combination of immediately actionable, already-approved components.
Full mechanistic analysis available under commercial agreement.
Request AccessA non-invasive therapeutic technique demonstrates the ability to actively promote nerve repair in MS lesions, offering potential disease-modifying benefit beyond current symptom management approaches.
Full mechanistic analysis available under commercial agreement.
Request AccessA common dysfunction has been identified as a shared pathway across several distinct chronic pain conditions. A drug already approved for a cardiac indication, with a relevant secondary channel-modulating property, could be repurposed to target this shared mechanism across multiple pain syndromes at once.
Full mechanistic analysis available under commercial agreement.
Request AccessFirst proposal to combine two glucose-lowering mechanisms with different temporal profiles specifically in pediatric Type 1 diabetes, aiming to prevent downstream cardiovascular-kidney-metabolic complications in younger patients.
Full mechanistic analysis available under commercial agreement.
Request AccessLupus patients show selective, rather than global, immune dysfunction against influenza vaccines. A temporary pause in a specific B-cell-depleting biologic before vaccination could allow immune recovery and dramatically improve vaccine response in this high-mortality population.
Full mechanistic analysis available under commercial agreement.
Request AccessA rare HSV neurological complication in HIV patients may be severely underdiagnosed due to clinician bias. An immune modulator with a documented dual role — suppressing autoimmune inflammation while enhancing antiviral immunity — combined with standard antiviral therapy represents a completely unexplored treatment strategy.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific iron-dependent cell death process is emerging as a central mechanism in Parkinson's neurodegeneration. An investigational nanoparticle approach combined with an approved iron chelator targets both systemic and local drivers of this process — never previously attempted in Parkinson's.
Full mechanistic analysis available under commercial agreement.
Request AccessAn approved antiepileptic and an approved sedative each independently address different hallmark pathologies of Alzheimer's disease — and have never been tested in combination. Both cross the blood-brain barrier with decades of established safety data, enabling a trial within 12 months.
Full mechanistic analysis available under commercial agreement.
Request AccessCombining a cholesterol-pathway antiviral approach with an intranasal immune-priming agent that bypasses the limitations of oral delivery attacks both viral replication and host immune defence simultaneously.
Full mechanistic analysis available under commercial agreement.
Request AccessHIV treatment failure is driven less by regimen complexity than by a specific, distinct psychological barrier around medication-taking behaviour. An approved antidepressant with a relevant mechanism could directly address this neurobiological pathway.
Full mechanistic analysis available under commercial agreement.
Request AccessA next-generation opioid selectively activates the pain-relief signalling pathway while avoiding the pathway responsible for respiratory depression and addiction. Combined with AI-driven real-time dosage optimisation, this could deliver effective chronic pain management without the danger that makes traditional opioids so risky.
Full mechanistic analysis available under commercial agreement.
Request AccessA chronic pelvic pain condition has a 90%+ treatment failure rate with current therapies. A specific inflammatory signalling molecule directly excites pain nerves through a pathway completely independent of inflammation itself. An approved anti-inflammatory biologic class could work as a direct analgesic — not by reducing inflammation, but by blocking nerve excitation at its source. Zero clinical trials have ever tested this despite clear mechanistic evidence.
Full mechanistic analysis available under commercial agreement.
Request AccessA widely prescribed MS drug class uses identical dosing regardless of patient age or sex, despite documented metabolic differences that produce systematic over- and under-dosing across patient groups. The pharmacokinetic data supporting stratified dosing has been published for over a decade. No formal trial has tested an age- and sex-stratified protocol as a primary endpoint, and no regulatory submission has been made. This is not a new drug — it is a precision correction to how an existing drug is already being used.
Full mechanistic analysis available under commercial agreement.
Request AccessPatients with a specific chronic liver condition show paradoxically enhanced vaccine responses due to elevated baseline inflammation. An approved gut-modulating antibiotic could deliberately pre-condition this inflammatory state before vaccination to optimise antibody production — inverting the standard assumption that inflammation impairs vaccine efficacy.
Full mechanistic analysis available under commercial agreement.
Request AccessAn FDA-approved COVID-19 antiviral targets an enzyme structurally homologous to one essential for rhinovirus replication. Zero studies have tested this despite the mechanistic overlap being directly demonstrable from structural data. A second, independently-acting antifungal agent offers additional combination potential.
Full mechanistic analysis available under commercial agreement.
Request AccessA neuropeptide driving migraine pain is now identified as a significant contributor to endometriosis-associated pelvic pain. An approved migraine biologic has never been tested in endometriosis despite targeting the same underlying pathway. A non-pharmacological nerve stimulation technique offers a complementary approach — a combination with zero prior research.
Full mechanistic analysis available under commercial agreement.
Request AccessLupus-related kidney damage has a newly identified mechanism distinct from the classical immune-complex model. An approved, widely available antioxidant compound directly inhibits this specific cell death cascade. Prior trials of this compound targeted oxidative stress generally — none have tested this specific mechanistic rationale.
Full mechanistic analysis available under commercial agreement.
Request AccessPeanut oral immunotherapy achieves desensitisation, but sustained remission remains elusive. Three mechanistically non-overlapping interventions — a biologic, a specific probiotic strain, and standard OIT — have each been tested individually or in pairs, but never all three together, despite acting through completely independent pathways.
Full mechanistic analysis available under commercial agreement.
Request AccessA drug approved for autoimmune disease and transplant rejection blocks one immune activation pathway, while a distinct T-cell engaging cancer therapy activates T-cells through a completely separate route — bypassing the blockade entirely. The two can be co-administered without sacrificing anti-tumour efficacy. Both approved. Zero prior trials combining them.
Full mechanistic analysis available under commercial agreement.
Request AccessLupus autoantibodies cross-react with a specific brain receptor via molecular mimicry, causing neuronal damage and the cognitive dysfunction that defines neuropsychiatric lupus. An approved Alzheimer's drug directly blocks the same receptor subtype, crosses the blood-brain barrier reliably, and has an established safety profile. Zero clinical trials despite 20 years of mechanistic evidence.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific psoriasis biologic's known infection risk is not a side effect — it is a pharmacodynamic inevitability of its mechanism, with published data identifying specific peak-risk time windows. Time-limited prophylaxis with an approved antifungal during these windows, rather than continuous or reactive treatment, has never been systematically studied despite being entirely predictable from the drug's known pharmacology.
Full mechanistic analysis available under commercial agreement.
Request AccessCurrent peanut oral immunotherapy uses fixed dosing schedules, despite well-established immune variability between patients and across time. A protocol using a validated immune readiness test to dynamically guide when doses are escalated, held, or reduced addresses this directly. Multi-source convergent evidence supports the proposed threshold. Immediately actionable within existing trial infrastructure with no new drug development required. No prior clinical trial has tested this adaptive approach.
Full mechanistic analysis available under commercial agreement.
Request AccessAdults are underserved by peanut oral immunotherapy because dose-related reaction rates are substantially higher than in children, driving dropout. An approved biologic, restricted specifically to the updosing phase, could preserve the tolerogenic immune response while suppressing the dangerous reactions that cause abandonment. No completed trial exists for this specific application in adults.
Full mechanistic analysis available under commercial agreement.
Request AccessA drug class already approved for diabetes, heart failure, and kidney disease has been identified for two distinct, unexplored indications — one via causal genetic evidence for a completely unrelated metabolic condition, the other for limb preservation following a specific vascular procedure where current amputation rates remain unacceptably high with no approved pharmacotherapy.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific programmed cell death pathway continuously releases material that triggers the type I interferon burst driving the entire lupus autoimmune cascade. Current treatments suppress this cascade downstream. An investigational inhibitor already has Phase II safety data in a different autoimmune condition, yet zero registered lupus trials exist despite the mechanistic logic being fully mapped.
Full mechanistic analysis available under commercial agreement.
Request AccessChildren under six represent the highest remission potential window for peanut oral immunotherapy. A biologic that prevents new IgE generation, rather than only neutralising existing IgE, offers a mechanistically distinct approach in this age group. No published trial exists for this specific combination despite the biologic being approved from six months of age.
Full mechanistic analysis available under commercial agreement.
Request AccessAn approved antimalarial attacks drug-resistant HSV through two completely independent pathways simultaneously, bypassing the resistance mechanisms that cause standard antivirals to fail. For millions of patients with resistant HSV, this could be the first genuinely new treatment option in decades.
Full mechanistic analysis available under commercial agreement.
Request AccessEndometriosis causes chronic pelvic pain through fibrotic scar-like tissue that medicine has largely failed to treat. An approved blood pressure medication class has well-documented anti-fibrotic effects in other organs via a shared pathway. This same mechanism could directly target adhesion formation driving endometriosis pain. Zero studies have tested this despite a mechanistically strong fit.
Full mechanistic analysis available under commercial agreement.
Request AccessHIV patients on antiretroviral therapy develop a premature ageing syndrome driven by mitochondrial dysfunction and accumulated aged cells causing systemic damage. A metabolic supplement restores mitochondrial function while a senolytic combination clears the accumulated aged cells. This triple approach addresses both cause and consequence — never studied together in HIV patients.
Full mechanistic analysis available under commercial agreement.
Request AccessA catastrophic diabetic complication causes spontaneous bone collapse through uncontrolled inflammatory destruction. An approved osteoporosis drug directly blocks the pathway driving this overactivation. In a hormonally deficient subgroup, concurrent hormone replacement restores the balance that normally protects bone. This dual mechanism has never been studied despite both pathways being independently documented.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific sequential pathway links environmental toxin exposure to sustained neuroinflammation in Parkinson's. An approved cancer drug that crosses the blood-brain barrier blocks a critical node in this cascade. Combined with a structured rehabilitation protocol, this could simultaneously reduce neuroinflammation and enhance motor learning.
Full mechanistic analysis available under commercial agreement.
Request AccessA widely available, decades-old OTC drug stabilises a specific misfolded protein linked to the most common known genetic risk factor for Parkinson's, affecting a meaningful proportion of patients. Proof-of-concept trial data already exists. The drug remains unlicensed for this use despite established safety data and a directly validated mechanistic target — a classic repurposing gap where commercial incentives have failed to drive regulatory development.
Full mechanistic analysis available under commercial agreement.
Request AccessA drug approved for two specific rare epilepsy syndromes directly modulates the exact channel function affected in a related channelopathy, via a distinct receptor mechanism. This is a mechanistically grounded extension into an adjacent genetic epilepsy with a directly demonstrable molecular overlap. Zero trials exist despite the established safety profile and direct molecular connection.
Full mechanistic analysis available under commercial agreement.
Request AccessA low-dose repurposing of an approved drug suppresses chronic neuroinflammation underlying post-exertional malaise, the defining and most debilitating ME/CFS symptom, via a mechanism distinct from its standard-dose use. Neuroinflammation is now measurable by imaging, providing a validated biomarker endpoint. No properly powered trial exists despite compelling rationale and an inexpensive, accessible intervention.
Full mechanistic analysis available under commercial agreement.
Request AccessOne tree nut allergen binds immune cells with exceptional affinity, producing higher reaction and dropout rates than peanut allergy during OIT. A biologic that reduces the immune priming driving this severity uses the identical pathway already implicated in peanut allergy — a direct mechanistic transfer. Zero tree nut-specific trials exist for this combination.
Full mechanistic analysis available under commercial agreement.
Request AccessA biologic approved for severe asthma blocks the very first epithelial alarm signal that initiates the entire allergic cascade, before any downstream immune signalling begins. As an OIT adjunct, this targets the cascade upstream of where existing adjuncts act — preventing reactions at their source rather than managing them downstream. Zero peanut OIT trials exist for this drug despite the pathway being well established in food allergy sensitisation.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific antiviral pathway defect is measurable and defines a distinct ME/CFS subtype driven by innate immune dysregulation. Earlier trials of an investigational immune modulator showed modest signals in unselected populations — the key gap is that biomarker-stratified trial design using this defect as a selection criterion has never been conducted, despite being mechanistically distinct from other approaches in this series.
Full mechanistic analysis available under commercial agreement.
Request AccessA sequential biologic protocol identified for peanut OIT surfaces simultaneously for tree nut OIT — with an even stronger mechanistic argument given the exceptional allergen affinity involved. The transition logic between the two biologics follows identical reasoning. Two conditions, same protocol, stronger case in tree nut. No tree nut-specific sequential biologic trial exists.
Full mechanistic analysis available under commercial agreement.
Request AccessRadiation therapy to the head and neck damages a specific nerve cluster, upregulating a pain-signalling neuropeptide and producing chronic pain in survivors — a population with no mechanism-targeted treatment. No drug in this class has ever been evaluated in radiation-induced pain despite the pathway being directly implicated by the same mechanism the drug already blocks in migraine.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific immune structural change begins forming earlier in MS than previously assumed — not only in progressive disease. One approved biologic depletes peripheral immune cells but cannot penetrate brain tissue; a second crosses the blood-brain barrier and suppresses the compartmentalised inflammation current therapies cannot reach. Combining them early, before this structure consolidates, could alter the long-term trajectory toward progressive MS.
Full mechanistic analysis available under commercial agreement.
Request AccessA shared allergenic protein family links reactivity across cashew, pistachio, and walnut — but this cross-reactivity has never been therapeutically exploited. Using a single purified component to desensitize patients to multiple tree nuts simultaneously, rather than treating each allergy separately, could dramatically simplify treatment for the large multi-nut-allergic population.
Full mechanistic analysis available under commercial agreement.
Request AccessDamaged heart tissue after a heart attack accumulates aging-related cells that actively suppress the heart's own limited regenerative capacity. Combining an emerging cardiac regeneration technique with agents that clear these regeneration-blocking cells targets two independent, non-overlapping barriers simultaneously — a combination with no prior research despite both approaches being independently validated.
Full mechanistic analysis available under commercial agreement.
Request AccessThe global shift to a specific integrase inhibitor backbone — now first-line in most countries — carries an underrecognised metabolic side effect affecting urate handling. The same inflammasome pathway implicated in this metabolic complication is independently activated in the neurological complications affecting an estimated 30–50% of virologically suppressed patients. A cheap, off-patent anti-inflammatory with an established safety record in cardiovascular trials targets both via a single mechanism. Zero trials exist testing this drug in this population despite the dual mechanistic rationale being directly derivable from published HIV pathophysiology.
Full mechanistic analysis available under commercial agreement.
Request AccessThe majority of colorectal cancers are effectively invisible to the immune system and do not respond to checkpoint inhibitors. A kinase inhibitor with an established clinical safety profile has been shown to trigger a specific form of cancer cell death that emits danger signals making tumour cells visible to the immune system. Combining it with a drug that simultaneously removes the “don’t eat me” signal from tumour cell surfaces creates a two-pronged approach attacking immune exclusion from independent angles. No trial has tested this specific combination in colorectal cancer despite both agents having existing clinical data in other settings.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific upstream signalling node is activated independently of TNF in rheumatoid synovial tissue, explaining why a meaningful subset of patients on TNF inhibitors achieve only partial response. An oral drug with an established safety database from trials in a neurological condition inhibits this node directly. Adding it to background TNF inhibitor therapy could convert partial responders into full responders via a complementary, non-overlapping mechanism. Zero RA trials exist for this drug despite the mechanistic rationale being fully mapped and a validated patient selection biomarker already available.
Full mechanistic analysis available under commercial agreement.
Request AccessTwo independent mechanistic opportunities have been identified in lupus nephritis — one targeting the complement-coagulation crosstalk driving concurrent thrombosis and kidney inflammation in a definable patient subgroup, the other targeting a cell-death pathway that amplifies kidney fibrosis independently of antibody-mediated damage. An approved drug for a related vasculitis condition has never been tested in lupus despite sharing the identical mechanistic target. A second combination — pairing an approved BAFF/APRIL inhibitor with an investigational inflammasome inhibitor — has no prior art in lupus whatsoever. Zero registered trials exist for either approach.
Full mechanistic analysis available under commercial agreement.
Request AccessA specific gastrointestinal complication of lupus lacks any targeted treatment despite causing significant morbidity. Patients with this complication show depleted levels of a gut-derived metabolite that, in mouse models, directly reverses the pathological tissue changes involved. The compound is low-toxicity, widely available, and no clinical trial has ever tested it for this application despite direct interventional evidence in preclinical models.
Full mechanistic analysis available under commercial agreement.
Request AccessMale adolescents on standard dolutegravir dosing show disproportionately higher rates of virologic failure compared to females and adults. An established liver enzyme pathway, upregulated specifically during male puberty, is predicted to reduce drug exposure below therapeutic levels during Tanner stages II-V. Two independent observational cohorts support the sex-specific failure signal. No pharmacokinetic study has tested this mechanism in adolescent males.
Full mechanistic analysis available under commercial agreement.
Request AccessA dietary intervention and a non-invasive brain stimulation technique each reduce seizure frequency through entirely different mechanisms — one via metabolic channel modulation, the other via synaptic plasticity adjustment. Both are independently validated across multiple RCTs. Their mechanisms are orthogonal, eliminating interaction risk. No trial has ever tested the combination despite the complementary biology being directly derivable from established neuroscience.
Full mechanistic analysis available under commercial agreement.
Request AccessRhinovirus infects nasal epithelial cells, then exploits compromised tight junctions to spread to deeper airway tissue. One approved nasal spray degrades the virion directly at the epithelial surface before attachment. A second compound, a tight junction protective peptide, blocks the basolateral spread that follows. The mechanisms are non-overlapping and target consecutive steps. No trial has tested this combination despite both components having established clinical or preclinical data.
Full mechanistic analysis available under commercial agreement.
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