• TR06693098 → possibility of PLsis-related findings in male after 3-days at ≥100 mg/kg, where Cmaxis 66,914 ng/mL and AUC0-24 is 1,238,167 ng*h/mL.
  • TR06980443 → No indications of PLsis-related findings in male after 3-days up to 600 mg/kg, where Cmaxis 119,000 ng/mL and AUC0-24 is 3,130,000 ng*h/mL.
    • In only one rat at 600 mg/kg, decrease in spontaneous movement and/or ataxia was found and the reason is unclear. Longer duration study (14-d tox) is needed to investigate this profile. Spontaneous movement and/or ataxia would be non-specific toxicity. This finding is visible due to TR098 dosing, and a certain number of similar symptoms will be seen if the number of animals is increased. Lower dose than 600 mg/kg should be selected for 14-d tox study.
    • Decrease of body temperature was observed in an animal (#4001) showing decrease in spontaneous movement at 1h after dosing, but the body temperature was recovered at 8h.
    • Muscle toxicity observed in the TR443 and TR993 toxicity studies (data is not available yet) was not observed in the TR098 toxicity study.
    • Phospholipidosis (PLsis)-related findings (vacuolation and foamy macrophage infiltrate) were detected in many organs of all animals of 600 mg/kg group. In the 100 mg/kg group, a few animals showed PLsis-related findings. Longer dosing periods would likely result in more animals showing symptoms of PLsis-related findings.
    • It was surprised that PLsis-related findings were detected in vivo rat minitox study of TR098, because TR098 the risk of PLsis of TR098 in vitro was low (23%). TR443 did not show the PLsis-related findings in vivo 3-d rats and the results of histopathology of in vivo rat 5-d tox for TR993 are ongoing.
    • to continue the investigation of TR098 as a CN candidate, and the safety profile of TR098 will be checked in 14-d tox study after CN.
주로 cationic amphiphilic drug (CAD) (lipophilic) 한 drug 들이Nonspecific binding to membrane phospholipids and uptake by acidic compartments (lysosomes)DIPL involves the trapping of drugs within the LE/Lys compartmentsaccumulation of drug-phospholipid complexes within lysosomal membranes.intracellular accumulation of myeloid bodies upon prolonged drug exposure↓ lysosomal functionNPC 닮아짐The risk of DIPL on human health is unknown. (although currently more than 250 drug candidates and marketed drugs have been reported to cause DIPL)
finding In vitro phospholipidosis fold-induction at 300uM: 098: 5.8 , 660: 15 Lysosomal trapping assay: Fa2N-4 (immortalized hepatocytes) liver is a lysosome rich organ.
Lysosomal trapping in Fa2N-4 accumulation ratio: 098: 5.8 , 660: 15
Suggestive findings* in ≥100 mg/kg in rat 3-day tox: Non-adverse vacuolation and foamy macrophage infiltrates likely associated with drug-induced phospholipidosis,
But no sign observed in brain!
There is currently inability to monitor DIPL routinely in clinic. The FDA formed Phospholipidosis Working Committee (PLWG), From regulatory perspective, DIPL has been considered an adverse finding whether justified or not.
plan assessment in 14-day DRFs
Assess in 9-week Atuka mouse study (IHC only)
Pending HED

Arthur: di-22:6-BMP as a biomarker of phospholipidosis {Liu, 2014 #2151}

  • Slight increases in ASL/ALT/ALP/GLDH were noted, but there were neither necrotic findings nor organ dysfunction in any organs
  • No findings in the nervous system
  • Can call non-adverse at this point but need to carefully check whether or not lesions would progress when dosing period is extended

“Generally, phospholipidosis occurs without any concurrent target organ toxicity or dysfunction and the general consensus is that phospholipidosis is an adaptive response, however, some regulators consider phospholipidosis as an adverse event since certain xenobiotics cause concurrent target organ toxicity and dysfunction.” https://journals.sagepub.com/doi/full/10.1177/0192623316672352

AnimalsSprague-Dawley Rats (Males, 10 weeks of age)
Test articleControl*TR06693098
Dose (mg/kg/day)030100600
Dose volume (mL/kg/day)5555
No. of animals3333
Mortality0000
Clinical signs---Decrease in spontaneous movement and/or ataxia# (#4001: 1 and 4h postdose on Day 3, and Day 4)
Body weights----
Food consumption----
Body temperature---↓ (1h)
Hematology----
Coagulation----
Blood chemistry-↓ Triglyceride
↑ AST, ALT, ALP, GLDH, Glucose, ↓ Calcium
Macroscopic examination----
Microscopic examination-- Vacuolation: Adrenal cortex, Foamy macrophage infiltration: Axillary/Inguinal/Submandibular lymph node, Lung
Stomach: Eosinophil infiltration, Thyroid: Follicular hypertrophy
Vacuolation: Renal proximal tubule, Hepatocyte/bile duct/Kupffer cell in the liver, Pancreatic acinar cell, Splenic lymphocyte, Foamy macrophage infiltration: Mesenteric lymph node, Spleen, Testis, Thymus
Stomach: Single cell necrosis of glandular epithelium, Mucosal hyperplasia, Edema in limiting ridge

Toxicokinetics parameters for TR0663098 (mean, n=3)

Parameter30100600
tmax (hr)Day 11.672.00
Day 31.333.67
Cmax (ng/mL)Day 120,08855,577
Day 323,20466,914
AUCτ (h*ng/mL)Day 1261,866874,406
Day 3356,6691,238,167

Day 3 (high-dose extension column): tmax 18.67 / 3.00 hr, Cmax 80,269 / 111,397 ng/mL, AUCτ 1,671,556 / 2,327,628 h*ng/mL.

Tissue concentrations of TR06693098 (mean, n=3)

Tissue30 mg/kg100 mg/kg600 mg/kg
CSF (ng/mL)123905
Liver (ng/g)26,654313,365
Brain (ng/g)2,41921,260

Extended (600 mg/kg post-extension column): CSF 6,227 ng/mL, Liver 4,652,897 ng/g.

[Clinical testing for DIPL]

  • Very good resosurce: Chatman (important) 2009: tiered strategy
  • Functional consequence: DIPL itself is not a direct toxic end point: 있어도 organ toxicity 없으면 갠찮고, organ toxicity 있어도 not 해: clinical monitoring plan, blood cell (wbc, smear, TEM), or
  • Consideration:
  • Critical organ? Neuron, heart, eye (all terminally differentiated)
  • Reversibility,
  • Biopsy & TEM
    • currently relies on the histopathological examination of tissue biopsies, bronchoalveolar lavage (BAL), peripheral blood cells (i.e. lymphocytes, neutrophils). Although TEM is considered the “gold standard” approach for determining DIPL, it is invasive, relatively non-quantitative, expensive and time-consuming. It may be difficult or not feasible to biopsy the tissues of interest (e.g. heart, brain, neurons).
  • peripheral blood cells & TEM
    • In clinical studies, peripheral blood cells may be more readily accessible for light microscopic and ultra-structural studies. However, the accuracy of blood cell testing would be based on the assumption that changes in peripheral cells reflect the extent of DIPL in other tissues.
    • The presence of PL in peripheral leukocytes is generally accepted as compound specific and is often predictive of PL in solid tissues. (… continued)
  • Regulatory
    • Black box warning example of Amiodarone: .. these changes also are present in approximately 50% of all patients on Cordarone therapy. These cells should be used as markers of theraphy, but not as evidence of toxicity.

Drugs (brand)ᵃ known to cause DIPL in animals

Drugs (brand)ᵃ known to cause DIPL in animalsDrug label/summaryᵇClinical case reportsReferences
DIPL in humansReported with concurrent toxicities
Antidepressant
  Citalopram (Celexa, Loxapram)
  Clomipramine (Anafranil)
  Duloxetine (Cymbalta)
  Fluoxetine (Prozac)Pulmonary toxicityGonzalez (...)
  Paroxetine (Paxil, Paroxetin)
Antipsychotic
  Chlorpromazine (Thorazine)Keratopathy, cataractWebber (...)
Antimalarial
  Amodiaquine (Camoquin, Flavoquine)Ocular changesHirst et al.
  Chloroquine (Aralen)Kidney toxicity, cardiotoxicity, keratopathy, retinopathy, myopathyJones et al. and Ro...
  Hydroxychloroquine (Plaquenil)Myopathy, kidney toxicityBolaños..., Khubchand...
  TafenoquineKeratopathyNasveld...
Antiviral
  Tilorone (Amixin IC)KeratopathyWeiss (...)
Antibiotic
  AmikacinKidney toxicityDeBroe (...)
  Azithromycin (Zithromax)
  Clarithromycin (BIAXIN)
  Gentamicin (Garamycin)Kidney toxicityDeBroe (...)
  Telithromycin (Ketek)
  Tobramycin (TOBI)Kidney toxicityDeBroe (...)
  TrimethoprimHepatotoxicityMuñoz (...)
Antifungal
  Posaconazole (Noxafil, Posanol)
Antimicrobial
  PentamidineLung toxicityFilippo (...)
Antiarrhythmic
  Amiodarone (Cordarone)Pulmonary toxicity, keratopathy, hepatotoxicity, neuropathy, kidney toxicityAdams (...)
  Dronedarone (Multaq)
Antianginal
  Perhexiline (Pexid)Hepatotoxicity, neuropathyBertrand (...)
  4,4'-diethylaminoethoxyhexesterol (Coralgil)Hepatotoxicity, pulmonary toxicity, splenomegalyYamamoto (...)
Statin
  RosuvastatinPulmonary toxicityLantuejoul (...)
  AtorvastatinPulmonary toxicityHuang (...)

(… drug list continues onto next photo)

Uncertain Spans

locationtranscriptionuncertainty
TR06980443 rowCmaxis 119,000 ng/mL and AUC0-24 is 3,130,000 ng*h/mL.The number 119,000 could read 119000 or 119000.0 depending on small comma resolution.
Reference columnGonzalez (...), Webber (...), etc.All cited author surnames are partially cropped at the right edge; only the first surname segment is read with confidence.
Tissue concentrations rowextension column 4,652,897 ng/gLast cell may include an additional unit suffix that is cropped.
Microscopic examination 600 mg/kg rowStomach: Single cell necrosis of glandular epithelium, Mucosal hyperplasia, Edema in limiting ridgeThe phrase Edema in limiting ridge could end with an additional word that is cropped.
Clinical testing bulletCritical organ? Neuron, heart, eye (all terminally differentiated)The trailing parenthetical is consistent across tile reads; one or two words may be cropped after differentiated.