What is the mechanism of action of this treatment?

Common treatments for Acute Kidney Injury (AKI) often target inflammation and cellular signaling pathways, which are crucial in the pathophysiology of the condition. For instance, Suramin, an investigational drug, inhibits multiple enzymes and receptors involved in cellular signaling and inflammation, potentially reducing the progression of AKI. Other treatments may include anti-inflammatory agents that mitigate the inflammatory response and protect renal function. These mechanisms are vital for AKI patients as they help to prevent further kidney damage, reduce the risk of progression to more severe stages of kidney disease, and improve overall outcomes.

What side effects are associated with this type of intervention?

Common treatments for Acute Kidney Injury (AKI) include medications like diuretics, ACE inhibitors, and angiotensin II receptor blockers. These treatments can have side effects such as electrolyte imbalances, hypotension, and renal toxicity. Specific to treatments like Suramin, which inhibits multiple enzymes and receptors, potential side effects may include gastrointestinal disturbances, hypersensitivity reactions, and hematologic abnormalities. Monitoring for these adverse effects is crucial to manage and mitigate risks effectively.

What prior FDA approvals exist?

There are no specific FDA-approved treatments for Acute Kidney Injury (AKI) that directly match the mechanism of action of Suramin, which inhibits multiple enzymes and receptors involved in cellular signaling and inflammation. Most treatments for AKI focus on supportive care, such as managing fluid balance, electrolytes, and addressing the underlying cause. Investigational therapies, including those targeting inflammation and cellular signaling pathways, are still under clinical evaluation.

What other types of research exist?

One promising alternative to Suramin for AKI treatment is the use of nanobodies targeting the P2X7 ion channel. Nanobodies have shown high potency in preventing IL-1β release, a key inflammatory mediator, making them a potential therapeutic option for inflammatory disorders like AKI. Another potential treatment is the use of small molecule modulators of GFRα/RET receptor signaling, such as XIB4035, which enhances receptor signaling and may offer a unique therapeutic approach for conditions involving inflammation and cellular damage.

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Antiparasitic Agent

Suramin for Acute Kidney Injury

Phase 2

Waitlist Available

Research Sponsored by Rediscovery Life Sciences

Eligibility Criteria Checklist

Specific guidelines that determine who can or cannot participate in a clinical trial

Must have

Be older than 18 years old

Timeline

Screening 3 weeks

Treatment Varies

Follow Up 7 days

Awards & highlights

Summary

This trial is testing suramin, a medication, to see if it can help people with acute kidney injury (AKI) avoid worsening kidney problems. The goal is to prevent their condition from progressing to a severe stage or needing dialysis. Suramin works by blocking harmful processes that can damage the kidneys.

Who is the study for?

Adults with early-stage acute kidney injury (AKI) who haven't responded to a diuretic called furosemide are eligible. They must not have severe liver issues, be on multiple blood pressure medications, or have certain infections like HIV or COVID-19. A negative pregnancy test is required for women of childbearing age.

What is being tested?

The study is testing Suramin against a placebo in patients with AKI to see if it can prevent worsening to Stage III AKI or the need for dialysis. Participants will be randomly assigned to receive either Suramin or a placebo without knowing which one they're getting.

What are the potential side effects?

While specific side effects of Suramin in this trial context aren't listed, common ones may include nausea, vomiting, fatigue, and possible allergic reactions. The severity and type of side effects can vary from person to person.

Timeline

Screening ~ 3 weeks3 visits

Treatment ~ Varies

Follow Up ~ 7 days

Screening ~ 3 weeks

Treatment ~ Varies

Follow Up ~7 days

This trial's timeline: 3 weeks for screening, Varies for treatment, and 7 days for reporting.

Treatment Details

Study Objectives

Study objectives can provide a clearer picture of what you can expect from a treatment.

Primary study objectives

To evaluate and compare the efficacy of a single 3.0 mg/kg infusion of suramin versus placebo in subjects with diuretic unresponsive AKI

Side effects data

From 2016 Phase 1 & 2 trial • 10 Patients • NCT02508259

100%

Rash

40%

Upper respiratory tract infection (URI)

40%

Hyperactivity

20%

Vomiting

20%

Hypoglycemia

20%

Headache

100%

80%

60%

40%

20%

Study treatment Arm

Suramin

Saline (Placebo)

Trial Design

2Treatment groups

Experimental Treatment

Placebo Group

Group I: SuraminExperimental Treatment1 Intervention

Group II: PlaceboPlacebo Group1 Intervention

Treatment

First Studied

Drug Approval Stage

How many patients have taken this drug

Suramin

2012

Completed Phase 3

~520

Do I qualify?Apply below to find out

Research Highlights

Information in this section is not a recommendation. We encourage patients to speak with their healthcare team when evaluating any treatment decision.

Mechanism Of Action

Side Effect Profile

Prior Approvals

Other Research

Common treatments for Acute Kidney Injury (AKI) often target inflammation and cellular signaling pathways, which are crucial in the pathophysiology of the condition. For instance, Suramin, an investigational drug, inhibits multiple enzymes and receptors involved in cellular signaling and inflammation, potentially reducing the progression of AKI. Other treatments may include anti-inflammatory agents that mitigate the inflammatory response and protect renal function. These mechanisms are vital for AKI patients as they help to prevent further kidney damage, reduce the risk of progression to more severe stages of kidney disease, and improve overall outcomes.

Contrast-induced acute kidney injury in interventional cardiology: Emerging evidence and unifying mechanisms of protection by remote ischemic conditioning.