Pariceract

Pariceract
Clinical data
Other namesBIA 28-6156; LTI-291; LIT291; LTI-00291
Routes of
administration		Oral
Drug classβ-Glucocerebrosidase (GCase) activator or positive allosteric modulator
Identifiers
  • 5,7-dimethyl-N-(4-pentoxycyclohexyl)pyrazolo[1,5-a]pyrimidine-3-carboxamide
CAS Number
PubChem CID
ChemSpider
UNII
Chemical and physical data
FormulaC20H30N4O2
Molar mass358.486 g·mol−1
3D model (JSmol)
  • CCCCCOC1CCC(CC1)NC(=O)C2=C3N=C(C=C(N3N=C2)C)C
  • InChI=1S/C20H30N4O2/c1-4-5-6-11-26-17-9-7-16(8-10-17)23-20(25)18-13-21-24-15(3)12-14(2)22-19(18)24/h12-13,16-17H,4-11H2,1-3H3,(H,23,25)
  • Key:HZILSILAELSWKN-UHFFFAOYSA-N

Pariceract (INNTooltip International Nonproprietary Name; developmental code name BIA 28-6156 or LTI-291) is a β-glucocerebrosidase (GCase) activator or positive allosteric modulator which is under development for the treatment of Parkinson's disease. It is taken orally. GCase is a lysosomal enzyme encoded by the gene GBA1. Loss-of-function mutations in this gene are thought to promote α-synuclein accumulation and are among the leading genetic risk factors for Parkinson's disease. As such, activation of GCase might provide a disease-modifying therapy for treatment of Parkinson's disease. Pariceract was first described in the scientific literature by 2017. It was originated by Lysosomal Therapeutics and is under development by Lysosomal Therapeutics and Bial. As of October 2025, it is in phase 2 clinical trials.

See also

References

  1. 1 2 3 4 5 "LTI 291". AdisInsight. Springer Nature Switzerland AG. 15 October 2025. Retrieved 19 February 2026.
  2. 1 2 3 "Delving into the Latest Updates on Pariceract with Synapse". Synapse. 8 May 2025. Retrieved 19 February 2026.
  3. 1 2 3 "Pariceract Drug Profile". Ozmosi. 1 January 1900. Retrieved 19 February 2026.
  4. 1 2 3 4 den Heijer JM, Kruithof AC, Moerland M, Walker M, Dudgeon L, Justman C, et al. (July 2023). "A Phase 1B Trial in GBA1-Associated Parkinson's Disease of BIA-28-6156, a Glucocerebrosidase Activator". Movement Disorders. 38 (7): 1197–1208. doi:10.1002/mds.29346. hdl:1887/3722043. PMID 37195859.
  5. 1 2 3 4 den Heijer JM, Kruithof AC, van Amerongen G, de Kam ML, Thijssen E, Grievink HW, et al. (September 2021). "A randomized single and multiple ascending dose study in healthy volunteers of LTI-291, a centrally penetrant glucocerebrosidase activator". British Journal of Clinical Pharmacology. 87 (9): 3561–3573. doi:10.1111/bcp.14772. PMC 8451761. PMID 33576113.
  6. 1 2 Ellis JM, Fell MJ (September 2017). "Current approaches to the treatment of Parkinson's Disease". Bioorganic & Medicinal Chemistry Letters. 27 (18): 4247–4255. doi:10.1016/j.bmcl.2017.07.075. PMID 28869077. Increased degradation of a-synuclein is another potential mechanism explored in the clinic. Currently, the leading candidates for this approach center on modulating the activity of the Glucocerebrosidase (GBA) pathway. Mutations in GBA are the leading genetic risk factor for sporadic PD and reductions in GBA activity are thought to lead to an accumulation of a-synuclein. Lysosomal Therapeutics is currently developing a brain penetrant, small molecule enhancer of GBA activity called LTI-291 (structure not reported) which is expected to enter Phase 1 testing in 2017.