Sequential CD73 Upregulation Before Glucocorticoids in SIRS

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Solution Overview

Problem

Simultaneous administration of glucocorticoids and type I interferons increases mortality in patients with conditions leading to Systemic Inflammatory Response Syndrome (SIRS) and Multiple Organ Dysfunction Syndrome (MODS), as glucocorticoids block the organ-protective effects of CD73 induction by type I interferons.

Innovation Solution

Administer an agent capable of up-regulating CD73, such as type I interferons, followed by glucocorticoids, in a sequential manner to induce organ protection and then dampen inflammation.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If glucocorticoids and type I interferons are administered simultaneously, then anti-inflammatory effects are achieved, but mortality increases due to blocked CD73 induction

Engineering Contradiction:

Improvemortality rateVSAvoidtreatment sequence complexity

Core Design Contradiction:

ReliabilityVSDevice complexity

Solution Approach 1:

The patent applies preliminary action by administering type I interferons before glucocorticoids. This sequence allows CD73 to be induced and up-regulated on endothelial cells prior to glucocorticoid administration, ensuring the organ-protective adenosine pathway is established before anti-inflammatory suppression begins. This temporal ordering resolves the contradiction by preventing the blocking effect while maintaining both therapeutic benefits.

Inventive Principle:

Principle #10Preliminary action

2Object-affected harmful factors

If glucocorticoids are administered early in the disease course, then inflammation is suppressed, but organ protection is reduced due to blocked CD73 expression

Engineering Contradiction:

Improveinflammation levelVSAvoidorgan protection

Core Design Contradiction:

Object-affected harmful factorsVSReliability

Solution Approach 1:

The patent implements preliminary action by establishing CD73 expression through type I interferon administration before initiating glucocorticoid therapy. This ensures that the endothelial cells have already up-regulated CD73 and are capable of producing protective adenosine, thereby preserving organ protection mechanisms even as glucocorticoids suppress inflammation.

Inventive Principle:

Principle #10Preliminary action

Solution Approach 2:

The treatment is segmented into distinct phases: first the induction phase with type I interferons to establish CD73 expression, then the suppression phase with glucocorticoids for inflammation control. This segmentation allows each agent to perform its optimal function without interference, resolving the contradiction between inflammation suppression and organ protection.

Inventive Principle:

Principle #1Segmentation

3Reliability

If type I interferons are used alone, then CD73 induction occurs providing organ protection, but excessive inflammation persists

Engineering Contradiction:

Improveorgan protectionVSAvoidinflammation level

Core Design Contradiction:

ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent merges two therapeutic approaches by combining type I interferons (for CD73 induction and organ protection) with glucocorticoids (for inflammation suppression). By administering them in the correct sequence rather than simultaneously or in reverse order, the combination achieves both organ protection and inflammation control, resolving the contradiction between these two beneficial effects.

Inventive Principle:

Principle #5Merging (Combining)

Applied Scientific Principles

This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.

Function Achieved in This Case

Reduces mortality and improves patient outcomes by ensuring CD73 induction before administering glucocorticoids, thereby protecting organs and reducing excessive inflammation.

Implementation Method 1

type I interferons have bound to their receptor IFNAR. One of these IFN-stimulated proteins is CD73. CD73 is a crucial enzyme and possibly one of the most conserved enzymes due to its role in the pathway in the metabolism in adenosine triphosphate (ATP) to adenosine.

Methodology Applied

Scientific EffectReceptor binding and gene induction:

Implementation Method 2

CD73 is a crucial enzyme and possibly one of the most conserved enzymes due to its role in the pathway in the metabolism in adenosine triphosphate (ATP) to adenosine. CD73 and CD39 are both involved in the breakdown, however CD73 is the rate limiting enzyme to this metabolism.

Methodology Applied

Scientific EffectEnzyme catalysis: Enzyme

Implementation Method 3

Adenosine is a potent anti-inflammatory and organ protective agent

Methodology Applied

Scientific EffectAnti-inflammatory signaling:

Data Source

PatentUS12472235B2Treatment of diseases with sequential administration of an agent capable of up-regulating CD73 and glucocorticoids

Publication Date: 2025.11.18 FARON PHARMA OY

AI summary

A method for preventing and/or treating systemic inflammatory response syndrome (SIRS), the method comprising administration of an agent capable of up-regulating CD73 in combination with a glucocorticoid and/or an agent capable of agonizing the glucocorticoid receptor, wherein an agent capable of up-regulating CD73 and a glucocorticoid and/or an agent capable of agonizing the glucocorticoid receptor are administered sequentially. An agent capable of up-regulating CD73 is administered prior to a glucocorticoid and/or an agent capable of agonizing the glucocorticoid receptor.