DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for potassium deficiency disease — screening already-approved drugs against its 20-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePotassium deficiency disease maps to a 20-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for potassium deficiency disease is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase (ABO) — ABO is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet 6-deoxy-alpha-l-galactopyranosyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4Y63 · 1.3 Å · ligand octyl 2-O-(6-deoxy-alpha-L-galactopyranosyl)-beta-D-galactopyranoside (BHE). Experimental structure, not a prediction.
What the evidence adds up to
A 1973 multi-centre study of 210 general practice patients with a mean age of 75 years assessed signs and symptoms of potassium deficiency before and after a potassium supplement (Slow-K, 8.06 mEq three times daily). After treatment, 86% of patients showed symptomatic improvement, and mean potassium levels rose from 3.8 to 4.4 mEq/l. Mean haemoglobin levels increased slightly from 12.1 to 12.8 g/100ml. The trial design did not allow conclusive correlation of symptomatic improvement with therapy.
Guidelines from 2000, developed by a multidisciplinary National Council on Potassium in Clinical Practice, recommend oral potassium replacement therapy when bowel sounds are present, except in life-threatening ventricular arrhythmias, digitalis intoxication, or paralysis. The plasma potassium concentration can serve as a rough index of body potassium stores in the absence of independent factors causing transcellular potassium shifts. Associated fluid and electrolyte disorders should be corrected, and causes of potassium loss identified and eliminated.
Management of hyperkalemia, a potentially lethal electrolyte disturbance, is reviewed in papers from 2008 and 2019. A physiologically based sequential approach applies, but each therapy carries risks. Simultaneous insulin and glucose administration is associated with frequent dysglycaemic complications. Beta-2 agonists carry potential for cardiac ischaemia and arrhythmias. Hypertonic sodium bicarbonate infusion in acidotic patients represents a large hypertonic sodium load. Renal replacement therapy is effective but invasive. Potassium-lowering drugs can cause rapid decreases in serum potassium, leading to cardiac hyperexcitability and rhythm disorders. Treatment should be tailored to the patient's condition.
In kidney transplant recipients, both hyperkalemia and hypokalemia are common, but consensus on management is lacking, particularly for hyperkalemia. After correcting emergencies, treatment includes correcting insulin deficiency, adjusting medications, and dietary counselling. Regular laboratory testing is essential because patients are often asymptomatic. What remains missing are prospective trials that stratify patients by aetiology of potassium disturbance, adequately powered to assess hard outcomes rather than surrogate electrolyte levels, and funded independently of commercial potassium supplement manufacturers.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Archives of Internal Medicine · 2000 · 313 citations
New Guidelines for Potassium Replacement in Clinical Practice
AbstractThis article is the result of a meeting of the National Council on Potassium in Clinical Practice. The Council, a multidisciplinary group comprising specialists in cardiology, hypertension, epidemiology, pharmacy, and compliance, was formed to examine the critical role of potassium in clinical practice. The goal of the Council was to assess the role of potassium in terms of current medical practice and future clinical applications. The primary outcome of the meeting was the development of guidelines for potassium replacement therapy. These guidelines represent a consensus of the Council members and are intended to provide a general approach to the prevention and treatment of hypokalemia.
AbstractBACKGROUND AND OBJECTIVES: Hyperkalemia is one of the few potentially lethal electrolyte disturbances. Prompt recognition and expeditious treatment of severe hyperkalemia are expected to save lives. This review is intended to provide intensivists and other interested clinicians with an understanding of the pathophysiology that underlies hyperkalemia, and a rational approach to its management. METHODS: This article reviews and analyzes literature relevant to the pathophysiology and management of severe hyperkalemia. Methods include search of MEDLINE, and bibliographic search of current textbooks and journal articles. RESULTS AND CONCLUSIONS: A more complete understanding of potassium homeostasis in recent years has led to new approaches to the management of severe hyperkalemia. The physiologically based sequential approach still applies. The efficacy, pitfalls, and risks of the agents available for use at each step in the sequence are critically reviewed. Rational use of the available tools will allow clinicians to successfully treat severe hyperkalemia.
Annals of Intensive Care · 2019 · 137 citations · open access
Management of hyperkalemia in the acutely ill patient
AbstractPURPOSE: To review the mechanisms of action, expected efficacy and side effects of strategies to control hyperkalemia in acutely ill patients. METHODS: We searched MEDLINE and EMBASE for relevant papers published in English between Jan 1, 1938, and July 1, 2018, in accordance with the PRISMA Statement using the following terms: "hyperkalemia," "intensive care," "acute kidney injury," "acute kidney failure," "hyperkalemia treatment," "renal replacement therapy," "dialysis," "sodium bicarbonate," "emergency," "acute." Reports from within the past 10 years were selected preferentially, together with highly relevant older publications. RESULTS: Hyperkalemia is a potentially life-threatening electrolyte abnormality and may cause cardiac electrophysiological disturbances in the acutely ill patient. Frequently used therapies for hyperkalemia may, however, also be associated with morbidity. Therapeutics may include the simultaneous administration of insulin and glucose (associated with frequent dysglycemic complications), β-2 agonists (associated with potential cardiac ischemia and arrhythmias), hypertonic sodium bicarbonate infusion in the acidotic patient (representing a large hypertonic sodium load) and renal replacement therapy (effective but invasive). Potassium-lowering drugs can cause rapid decrease in serum potassium level leading to cardiac hyperexcitability and rhythm disorders. CONCLUSIONS: Treatment of hyperkalemia should not only focus on the ability of specific therapies to lower serum potassium level but also on their potential side effects. Tailoring treatment to the patient condition and situation may limit the risks.
AbstractFor successful potassium replacement, one should consider the optimal potassium preparation, route of administration, and the appropriate speed of administration. In the absence of an independent factor causing transcellular potassium shifts, the plasma potassium concentration can be used as a rough index to estimate body potassium stores. Oral KCl replacement therapy is preferable if there are bowel sounds, except in the setting of life-threatening abnormalities such as ventricular arrhythmias, digitalis intoxication, or paralysis. In patients with impaired renal function or those treated with intravenous potassium, the risk of hyperkalemia should be monitored. Since potassium depletion rarely occurs as an isolated phenomenon, associated fluid and electrolyte disorders should be corrected, and the causes of potassium loss should be sought and eliminated to complete the treatment of hypokalemia.
Current Medical Research and Opinion · 1973 · 5 citations
A multi-centre study of potassium deficiency in the elderly
AbstractSummaryTwo-hundred and ten patients from general practice with a mean age of 75 years were assessed for the signs and symptoms of potassium deficiency, before and after receiving a potassium supplement (‘Slow-K’) 8.06 mEq. three times a day. The assessment included potassium and haemoglobin levels, diet, and symptomatic ratings. Following treatment, 86% of patients showed symptomatic improvement, and there was a highly significant increase in mean potassium levels from 3.8 to 4.4 mEq./l. Interestingly there was a slight but significant increase in mean haemoglobin levels from 12.1 to 12.8 g./100ml. It was not possible, because of the trial design, to correlate conclusively the symptomatic improvement with the therapy.
World Journal of Transplantation · 2024 · 1 citations · open access
Disorders of potassium homeostasis after kidney transplantation
AbstractDisturbances of potassium balance are often encountered when managing kidney transplant recipients (KTR). Both hyperkalemia and hypokalemia may present either as medical emergencies or chronic outpatient abnormalities. Despite the high incidence of hyperkalemia and its potential life-threatening implications, consensus on its management in KTR is lacking. Hypokalemia in KTR is also well-described, although it is given less attention by clinicians compared to hyperkalemia. This article discusses the etiology, pathophysiology and management of both types of potassium disorders in KTR. Once any emergent situation has been corrected, treatment approaches include correcting insulin deficiency if present, adjusting non-immunosuppressive and immunosuppressive medications, eliminating or supplementing potassium as needed, and dietary counselling. Although commonly of multifactorial etiology, ascertaining the specific cause in a particular patient will help guide successful management. Monitoring KTR through regular laboratory testing is essential to detect serious disturbances in potassium balance since patients are often asymptomatic.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
