Brian Levy

www.inflammx.com

Clinical stage company developing an orally administered compound to inhibit the dysregulated NLRP3 Inflammasome pathway of autoinflammation. Indications: Diabetic Macular Edema (DME) secondary to Diabetic Retinopathy (DR), Chronic Kidney Disease secondary to Diabetic Nephropathy (DN) and the Intermediate form of Age Related Macular Degeneration (AMD). Phase 2 asset (Xiflam) planning to be in clinical trials in 2022. Patients will be dosed once a day with Xiflam or Placebo tablets. The objective of InflammX technology is disease modification through inhibiting the dysregulated NLRP3 Inflammasome by normalizing pathological prematurely open hemichannels in the cell membrane. These pathologically open Cx43 hemichannels release ATP into the extracellular space which is a signal for activation of the NLRP3 Inflammasome and release of multiple proinflammatory cytokines. This results in perpetuated autoinflammation in the clinically indicated diseases mentioned above. Xiflam has been shown to inhibit the pathologically open hemichannels resulting in reduced inflammation and tissue regeneration. in phenotypical models of the disease. Peer reviewed literature on the inflammasome supports the Cx43 mechanism as an activator of the NLRP3 inflammasome and drugs such as Xiflam being effective in multiple disease states.

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Clinical stage company developing an orally administered compound to inhibit the dysregulated NLRP3 Inflammasome pathway of autoinflammation. Indications: Diabetic Macular Edema (DME) secondary to Diabetic Retinopathy (DR), Chronic Kidney Disease secondary to Diabetic Nephropathy (DN) and the Intermediate form of Age Related Macular Degeneration (AMD). Phase 2 asset (Xiflam) planning to be in clinical trials in 2022. Patients will be dosed once a day with Xiflam or Placebo tablets. The objective of InflammX technology is disease modification through inhibiting the dysregulated NLRP3 Inflammasome by normalizing pathological prematurely open hemichannels in the cell membrane. These pathologically open Cx43 hemichannels release ATP into the extracellular space which is a signal for activation of the NLRP3 Inflammasome and release of multiple proinflammatory cytokines. This results in perpetuated autoinflammation in the clinically indicated diseases mentioned above. Xiflam has been shown to inhibit the pathologically open hemichannels resulting in reduced inflammation and tissue regeneration. in phenotypical models of the disease. Peer reviewed literature on the inflammasome supports the Cx43 mechanism as an activator of the NLRP3 inflammasome and drugs such as Xiflam being effective in multiple disease states.

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Country

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State

California

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City (Headquarters)

San Diego

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Employees

1-10

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Founded

2020

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