Dementia is the most common neurodegenerative disorder and is accompanied by a decline in intellectual functions such as memory, judgment, and language, as well as impairments in daily living, personality and behavior. Alzheimer dementia accounts for over 60% of all dementia patients and is known to be due to amyloid beta plaque and tau protein dysfunction in the brain. As of 2015, there were about 46.8 million people with dementia worldwide, with new diagnosed patient in every three seconds. The number of patients is doubling every 20 years and is expected to be 135 million by 2050.

In the early stages of Alzheimer's dementia, amyloid beta plaques (senile plaque) are formed in the brain, and after considerable progress, neurofibrillary tangles (NFT) are formed due to hyperphosphorylation of tau protein in neurons. Next, neurological inflammation occurs, which leads to brain damage, contractions, and dementia symptoms such as mild cognitive impairment and memory loss. We have already developed ¹⁸F-FC119S (Alzavue®) for imaging amyloid beta plaque and received new drug approval from Korean FDA in 2018. This drug can be used to detect amyloid beta plaques in the brain before dementia symptoms occur to ensure proper treatment. To date, there have been no treatments to improve Alzheimer's dementia symptoms or improve cognitive ability. That is the reason why amyloid beta diagnosis through PET imaging is important, because there are drugs to slow the progression of dementia or maintain neurotransmission ability.

The formation of neurofibrillary tangles in neurons by the tau protein occurs after the amyloid beta plaques, which is closer to the actual period that symptoms of dementia occur. Therefore, neurofibrillary tangle formation is attracting attention as a disease marker closer to actual dementia symptoms, and selective tau-PET drugs are being developed. A study has been reported that ¹⁸F-AV1451 and ¹⁸F-THK5351, which were early developed as tau-PET compounds, are unfortunately strongly bound to the proteins MAO-A and MAO-B in the brain (off-target binding), in addition to neurofibrillary tangles. This raised the problem that the brain-PET images obtained with these drugs may be images of other than neurofibrillary tangles, which makes it difficult to dementia diagnosis. In case of ¹⁸F-THK5351, development was totally terminated because it was found to bind more strongly to MAO-B than NFTs. In addition, Merck's ¹⁸F-MK6240 and Janssen's ¹⁸F-JNJ311 have recently emerged as new tau-PET candidates and have proven to be significantly superior to earlier compounds. Also, these drugs were proven to have no off target binding problems raised in ¹⁸F-AV1451 and ¹⁸F-THK5351, suggesting that selective NFT images can be provided. As a result of this research, Tau-PET R&D has entered the 2nd round worldwide. However, to date, Alzheimer's dementia has been shown to be driven by a very complex mechanism, making it increasingly difficult to evaluate new compounds in the basic research level.

Based on the previous literature, a number of compounds that are expected to selectively bind to NFTs have been designed and synthesized. Compound evaluation is performed using post-mortem brain tissue of Alzheimer's dementia patients and various screening methods. FC211 has no binding ability between amyloid beta, MAO-A and MAO-B, and has selective binding affinity only to NFT. Currently, imaging studies using animal models and pharmacokinetic studies are being conducted.