[11] The U.S. Securities and Exchange Commission (SEC), the U.S. National Institutes of Health (NIH), and City University of New York (CUNY) were also investigating whether Cassava or individuals manipulated data.

In 2012, they stated in The Journal of Neuroscience that the compound PTI-125 disrupted FLNA linkage with the alpha 7 nicotinic receptor as well as the toxic signaling of Abeta42, presenting PTI-125 as a novel therapeutic strategy for Alzheimer's disease.

[20] They later demonstrated, by isoelectric focusing, that simufilam restores to normal an altered conformation of FLNA in Alzheimer's disease models or postmortem human brain tissue.

[8] The U.S. Securities and Exchange Commission (SEC), the U.S. National Institutes of Health (NIH), and City University of New York (CUNY) were also investigating allegations of manipulated data.

[12] In October 2023, a leaked CUNY report indicated that they could obtain none of Wang's original data, which meant that they were unable to either prove or disprove allegations that the images were improperly manipulated;[9][32] they paused the investigation a few weeks later over concerns about confidentiality and integrity of the process.

[33] Research papers demonstrating the mechanism of action of simufilam contained an error of units in methods (one instance of milligrams noted as micrograms) and erroneous duplication of images, but neither journal found evidence of data manipulation that was previously alleged.

"[5] Robert Howard, professor of psychiatry at the University College London, is concerned on the lack of placebo and small sample size and said that the research "at the very least is implausible".

Thomas C. Südhof, Nobel laureate neuroscientist at Stanford University, also commented: "The overall conclusions with regard to Alzheimer's disease make no sense to me whatsoever... [The findings of Burns and Wang] are not in the mainstream of the field, and to me they seem implausible and contrived.