Disease-Phase Geometric Pharmacology of NRICM101 and NRICM201: Early Viral Suppressor vs Host-Rescue Attractor — A Unified TCM Systems Framework (v5)

This paper presents the v5 (strengthened) version of the disease-phase geometric pharmacology framework for NRICM101 (Qinguan No.1) and NRICM201 (Qinguan No.2). The central thesis: NRICM101 manages how the virus initiates disease (early viral-phase formula, Phase I-III); NRICM201 manages how the host loses control (severe host-rescue formula, Phase IV-VII). The transition between them is a pharmacological phase transition, not a dose escalation. Three new evidence tables added in v5: (1) Table 1 — systematic 8-axis comparison of NRICM101 vs NRICM201 pharmacological architecture, including expected biomarkers and cross-disease implications; (2) Table 2 — NRICM101 broad-spectrum antiviral mechanism as shared host pathological phase space coverage across SARS-CoV-2, influenza A, RSV, and Hantavirus, clarifying that cross-virus efficacy operates at the host level, not through direct viral protein inhibition; (3) Table 3 — NRICM201 host-rescue cross-disease evidence table across severe COVID-19, COPD, viral MOF, LPS/sepsis, acetaminophen liver failure, and Hantavirus severe phase, unified by the pathological inflammatory attractor theory. The Hantavirus external validation case demonstrates the framework's predictive power: Hantavirus lacks Mpro, rendering NRICM101 Jun cluster inactive, while its Phase IV-VII-dominant pathology maps directly to NRICM201 territory. This falsifiable prediction distinguishes the phase-specific framework from non-specific broad claims.