A process for preparing a compound of Formula (1a):

##STR00001##

or a pharmaceutically acceptable salt thereof.

The present embodiment provides a compound represented by the formula (1):
Q-CHR.sub.2  (1)
(Q is a nitrogen-containing aliphatic group containing two or more tertiary nitrogens but no oxygen, and R is an aliphatic group containing a biodegradable group). From the compound in combination with other lipids such as a lipid capable of reducing aggregation, lipid particles can be formed. Further, the compound can be used for a pharmaceutical composition to deliver an activator into cells.

It is intended to provide a novel method for treating a cancer using an FGFR inhibitor that exhibits a remarkably excellent antitumor effect and has fewer side effects. The present invention provides a combination preparation for the treatment of a malignant tumor comprising a compound represented by Formula (I) or a pharmaceutically acceptable salt thereof, and one or more additional compound(s) having an antitumor effect or pharmaceutically acceptable salt(s) thereof, and a pharmaceutical composition comprising both the active ingredients. The present invention also provides an antitumor effect enhancer, an antitumor agent, a kit for malignant tumor treatment, etc. comprising a compound represented by Formula (I) or a pharmaceutically acceptable salt thereof.

The invention provides compositions and methods for treating optic neuropathic disorders.

Provided is a new application of a chemokine receptor CCR6 inhibitor in preventing the recurrence of psoriasis. Specifically, provided is a use of the chemokine receptor CCR6 inhibitor for preparing a preparation or composition that is administered to a subject so as to prevent the recurrence of psoriasis in the subject. Also provided is a pharmaceutical product that prevents the recurrence of psoriasis. Using the provided drug products may effectively prevent or alleviate the recurrence of psoriasis.

Embodiments of the disclosure include methods and compositions useful for treating cancer in an immunogenic manner so as to elicit local tumor regression, while priming systemic immunity. In one embodiment, there is expansion of tumor-specific immune cells through administration of fibroblasts, either natural or modified in an intratumoral and/or peritumoral manner. In other embodiments, manipulation of a local tumor microenvironment is achieved by injections of immune-modulating fibroblasts to facilitate expansion of immune effector cells, which are subsequently re-stimulated in the periphery by antigenic exposure. In another embodiment, agents are provided that allow for systemic derepression of immunity, while optionally augmenting ability of immune effector cells to expand and kill tumor cells.

Provided are methods of treating cancer (e.g., a hematological cancer such as myelodysplastic syndrome) that comprise administering a polypeptide (e.g. a fusion polypeptide) that comprises a SIRPα D1 domain variant and an Fc domain variant in combination with a hypomethylating agent (e.g., azacitidine). Also provided are related kits.

The present disclosure provides pharmaceutical combinations comprising at least one spliceosome modulator and at least one inhibitor chosen from BCL2, BCL2/BCLxL, and BCLxL inhibitors. Also provided are methods of treating cancer comprising administering a therapeutically effective amount of at least one spliceosome modulator and a therapeutically effective amount of at least one inhibitor chosen from BCL2, BCL2/BCLxL, and BCLxL inhibitors.

The invention relates to Polθ inhibitors for use in the treatment of a cancer associated with a Shieldin deficiency and to pharmaceutical compositions comprising said Polθ inhibitors.

Provided is a method for predicting sensitivity of a cancer cell to a helicase inhibitor, the method comprising the step of: predicting a cancer cell having at least one mutation detected selected from the first group consisting of TTK mutation and RAD 50 mutation, as having sensitivity to a helicase inhibitor, or predicting a cancer cell having at least one mutation detected selected from the second group consisting of RAD 50 mutation, MRE 11 mutation, NBN mutation, DNA 2 mutation and RBBP 8 mutation, as having sensitivity to a helicase inhibitor.