mCPP is thought to be formed from nefazodone specifically by CYP2D6.The ratios of brain-to-plasma concentrations of mCPP to nefazodone are 47:1 in mice and 10:1 in rats, suggesting that brain exposure to mCPP may be much higher than plasma exposure. Conversely, hydroxynefazodone levels in the brain are 10% of those in plasma in rats. As such, in spite of its relatively low plasma concentrations, brain exposure to mCPP may be substantial, whereas that of hydroxynefazodone may be minimal. Chemistry
Nefazodone is a phenylpiperazine; it is an alpha-phenoxyl derivative of etoperidone which in turn was a derivative of trazodone. History
Nefazodone was discovered by scientists at Bristol-Myers Squibb (BMS) who were seeking to improve on trazodone by reducing its sedating qualities.BMS obtained marketing approvals worldwide for nefazodone in 1994. It was marketed in the US under the brand name Serzone and in Europe under the brand name Dutonin.In 2002 the FDA obligated BMS to add a black box warning about potential fatal liver toxicity to the drug label. Worldwide sales in 2002 were $409 million.In 2003 Public Citizen filed a citizen petition asking the FDA to withdraw the marketing authorization in the US, and in early 2004 the organization sued the FDA to attempt to force withdrawal of the drug. The FDA issued a response to the petition in June 2004 and filed a motion to dismiss, and Public Citizen withdrew the suit.Generic versions were introduced in the US in 2003 and Health Canada withdrew the marketing authorization that year.Sales of nefazodone were about $100 million in 2003.
Other common symptoms include;

clouding of the eyes natural lens
increase in intraocular pressure, which lies behind the iris and the pupil
red eyes
acute onset pain
tearing
corneal edema
photophobia (experience of discomfort to the eyes because of the exposure of high levels of light or by presence of physical sensitivity within the eyes)
significantly decreased vision.The major influencers of this illness include high exposure to the sun and age as this is a rare condition for individuals under the age of 35. Causes
Cataracts, if left untreated, can develop into a mature state or hyper mature state, and may progressively become leaky thereby excreting proteins. Cataracts are caused by a breakdown of proteins which allows the lens to become cloudy and gradually turn opaque, causing a decrease in vision. Through the leakage of proteins that have a high molecular weight an obstruction of the drainage mechanism of the eye is caused. Diagnosis
A variety of procedures can be used to physically diagnose phacolytic glaucoma as there are a variety of other types of glaucoma which may be confused with phacolysis such as acute angle-closure glaucoma (AACG), lens-particle glaucoma, neovascular glaucoma, phacomorphic glaucoma and uveitic glaucoma which can cause confusion in which procedures need to be conducted to revamp vision.The first type of diagnostic procedure referred to as a ‘slit lamp examination’ of phacolytic glaucoma allows for specific identification of microcystic corneal edema and the presence of macrophages, white material (dotted with patches within the inside capsule of the lens) and intense flare and iridescent or hyper-refringent particles specific to phacolytic glaucoma.